Immunology

GEB327

1. Course Contents

Shilu sir

Suhani mam

Full set q.

1.Introduction to Immune System: Adaptive and innate immunity, cells of the immune system, soluble mediators of immunity, cytokine, antigens, haptens
and carriers, immune responses, inflammation, opsonization, chemotaxis, phagocytosis, defense against intracellular and extracellular pathogens.

2. Cells and Organs Involved in Immune Responses(SS): lymphocytes (T-cells, B cells, NK cells), mononuclear phagocytes,
polymorphonuclear granulocytes, mast cells, platelets, antigen presenting cell, primary and secondary clonal expansion of lymphocytes.

3.The Humoral Immune Response(SM): Antigen-antibody interactions, affinity and avidity; antibodies, classification, structure, function and mechanism
of action; interferons and their functions.

4. The cell-mediated Immune Response(SS): Recognition of antigen by T cells, antigen presentation, the major histocompatibility complexes or
MHC molecules, the role of cytokines and the regulation of immune responses.

5. Complements(SM): Activities of complement proteins, activation of complement, classical pathway, regulation of classical pathway activation, alternative pathway,
activation and amplification loop, their regulation, membrane attack complex, biological effects of complement.

6. Immunity to Infection(SM): Immunity to intracellular and extracellular bacteria, viral infections, and parasitic infections.
7. Antigen Recognition(SS): antigen-antibody binding, antibody affinity and avidity, antibody specificity and cross reactivity, antigen processing and presentation, T-cell
antigen recognition.

8. Cell Cooperation in the Antibody Response: cooperation between different cell types, cell activation, antigen specific triggering of
lymphocyte, antibody responses in vivo, affinity maturation, immunological memory.

9. Immunopathology and Psychoneuroimmunology(SS): Immunodeficiency (AIDS), hypersensitivity, autoimmune disease,

immune-neuroendocrine network, endocrine-immune modulation, neuro-immune modulation, neuroendocrine and immune effect of psychosocial stress, effect of
psychosocial stress on infection, allergy, cancer, AIDS and autoimmunity, immune activity and psychopathology, immune function enhancement.

10. Immunological Techniques:

Chapterwise Q/A

1.Introduction to Immune System: Adaptive and innate immunity, cells of the immune system, soluble mediators of immunity, cytokine, antigens, haptens and carriers, immune responses,
inflammation, opsonization, chemotaxis, phagocytosis, defense against intracellular and extracellular pathogens.

1. What do you know about defense system ?

The immune system is the body's defense against infection. It is made up of a network of cells, tissues,
and organs that work together to protect the body from harmful substances and organisms.
The immune system has two main parts: the innate immune system and the adaptive immune system.

1. The innate immune system is the body's first line of defense against infection. It includes physical
barriers, such as the skin and mucous membranes, and chemical defenses, such as stomach acid
and lysozyme. The innate immune system also includes cells that can engulf and destroy harmful
substances, such as macrophages and neutrophils.
2. The adaptive immune system is the body's second line of defense against infection. It is activated
when the innate immune system is unable to clear an infection. The adaptive immune system is
more specific than the innate immune system and can recognize and attack a wider range of
harmful substances and organisms.

The adaptive immune system has two main components: B cells and T cells. B cells produce antibodies,
which are proteins that can bind to and neutralize harmful substances. T cells can attack and destroy
infected cells.

The immune system is a complex system that is constantly working to protect the body from infection.
When the immune system is not working properly, it can lead to a variety of diseases, including
autoimmune diseases, allergies, and infections.

Here are some of the defense mechanisms in immunology:

1. Physical barriers: The skin and mucous membranes are physical barriers that protect the body
from infection. The skin is a tough, waterproof layer that prevents harmful substances from
entering the body. The mucous membranes line the respiratory, digestive, and reproductive
tracts and produce mucus, which traps harmful substances and helps to remove them from the
body.
2. Chemical defenses: The body produces a variety of chemicals that help to fight infection.
Stomach acid kills harmful bacteria that are ingested. Lysozyme is an enzyme that breaks down
the cell walls of bacteria.
3. Phagocytosis: Phagocytes are cells that engulf and destroy harmful substances. Macrophages
and neutrophils are phagocytes that are found in the blood and tissues.
4. Inflammation: Inflammation is a response to injury or infection. It is characterized by redness,
swelling, heat, and pain. Inflammation helps to remove harmful substances from the body and
to repair damaged tissue.
5. Antibodies: Antibodies are proteins that are produced by B cells. Antibodies bind to specific
antigens, which are molecules that are found on the surface of harmful substances. Antibodies
can neutralize harmful substances, help to remove them from the body, and signal other
immune cells to attack them.
6. T cells: T cells are a type of white blood cell that play a role in the adaptive immune response. T
cells can attack and destroy infected cells and can help to regulate the immune response.

The immune system is a complex and dynamic system that is constantly working to protect the body
from infection. By understanding how the immune system works, we can develop better ways to prevent
and treat diseases.

2. Describe physiological functions of immune system.

The physiological functions of the immune system are to:

 1. Protect the body from foreign invaders, such as bacteria, viruses, parasites, and fungi.
2. Remove harmful substances from the body, such as toxins and allergens.
3. Repair damage to the body caused by infection or injury.
4. Fight cancer cells.
5. Regulate the immune response to prevent it from becoming too strong or too weak.

The immune system is a complex system that is made up of many different cells, tissues, and organs.
These work together to protect the body from harm.

Here are some of the specific physiological functions of the immune system:

1. **Physical barriers:** The skin is the body's largest physical barrier. It is a tough, waterproof
layer that helps to prevent bacteria and viruses from entering the body. The mucous membranes
that line the respiratory, digestive, and reproductive tracts also act as physical barriers.
2. **Chemical defenses:** The body produces a number of chemical defenses that help to kill
bacteria and viruses. These include stomach acid, lysozyme, and complement proteins.
3. **White blood cells:** White blood cells are the body's main defense against infection. There
are two main types of white blood cells: phagocytes and lymphocytes. Phagocytes engulf and
destroy bacteria and viruses. Lymphocytes produce antibodies, which help to fight infection.
4. **Antibodies:** Antibodies are proteins that bind to specific antigens. Antigens are molecules
that are found on the surface of bacteria, viruses, and other foreign invaders. When an antibody
binds to an antigen, it triggers a series of events that lead to the destruction of the invader.
5. **Inflammation:** Inflammation is a process that helps the body to heal itself. It is caused by
the release of chemicals from damaged cells and white blood cells. These chemicals cause
redness, swelling, heat, and pain. Inflammation helps to remove damaged cells and foreign
invaders from the body.
6. **Memory:** The immune system has a memory. This means that it can remember specific
invaders and produce a faster and stronger response the next time they are encountered. This is
why people who have been infected with a disease are often immune to it for a second time.

The immune system is a complex and dynamic system that is constantly working to protect the body
from infection. By understanding how the immune system works, we can develop better ways to prevent
and treat disease.

3. What do you know about PRRs ? " The innate immune system does not react against the host " -
Explain the statement .

Pattern recognition receptors (PRRs) are proteins that are found on the surface of cells of the innate
immune system. They recognize molecules that are common to pathogens, such as bacteria and viruses.
When a PRR binds to a pathogen, it triggers a series of events that lead to the destruction of the
pathogen.
The innate immune system does not react against the host because PRRs are designed to recognize
molecules that are common to pathogens. These molecules are not found on the surface of healthy cells,
so the innate immune system does not attack them.

###There are several types of PRRs, each of which recognizes a different type of molecule. Some of the
most important PRRs include:

1. Toll-like receptors (TLRs): TLRs recognize molecules that are found on the surface of bacteria and
viruses.
2. C-type lectin receptors (CLRs): CLRs recognize molecules that are found on the surface of fungi
and parasites.
3. NOD-like receptors (NLRs): NLRs recognize molecules that are released by damaged cells.

The innate immune system is the body's first line of defense against infection. It is important because it
can quickly respond to infection and prevent the pathogen from causing disease.

4. How haptens can be used in the study of antigenicity ?

Haptens are small molecules that cannot elicit an immune response on their own, but can do so when
attached to a larger carrier molecule. This is because the carrier molecule provides the hapten with the
necessary structure to be recognized by the immune system.

Haptens can be used to study antigenicity in a number of ways.

1. One way is to use haptens to identify the epitopes of antigens. Epitopes are the parts of an
antigen that are recognized by the immune system. By identifying the epitopes of an antigen,
scientists can learn more about how the immune system responds to that antigen.
2. Haptens can also be used to study the mechanisms of immune responses. For example,
scientists can use haptens to study how antibodies bind to antigens. They can also use haptens
to study how the immune system produces antibodies.
3. Haptens can also be used to develop new vaccines and drugs. For example, scientists can use
haptens to develop vaccines that protect against diseases caused by bacteria or viruses. They
can also use haptens to develop drugs that treat autoimmune diseases.

Overall, haptens are a valuable tool for studying antigenicity. They can be used to identify epitopes,
study the mechanisms of immune responses, and develop new vaccines and drugs.

5. What is phagocytosis ? Write down the molecular mechanism of phagocytosis . 1-4

Phagocytosis is a vital process by which certain cells of the immune system, called phagocytes, engulf
and internalize foreign particles, such as bacteria, cellular debris, or other pathogens. The molecular
mechanism of phagocytosis involves several steps:

1. Chemotaxis and Recognition: Phagocytosis is initiated by the attraction of phagocytes to the site
of infection or inflammation through chemotaxis. Chemical signals, such as cytokines or
molecules released by pathogens, attract phagocytes to the site. Once at the site, phagocytes
recognize foreign particles by sensing specific molecules on their surface, such as pathogen-
associated molecular patterns (PAMPs).
 2. Attachment: The phagocyte's surface receptors, known as pattern recognition receptors (PRRs),
interact with the PAMPs on the surface of the foreign particle. This binding triggers signaling
events that promote the formation of pseudopods, which are temporary extensions of the cell
membrane.
3. Engulfment: The pseudopods surround the foreign particle, gradually enclosing it within a
phagocytic cup or phagosome. This process is aided by actin polymerization, where the actin
cytoskeleton rearranges to provide mechanical support and driving force for the engulfment
process.
4. Phagosome Formation: The phagocytic cup closes completely, resulting in the formation of a
phagosome, which is a membrane-bound vesicle containing the internalized particle. The
phagosome separates from the plasma membrane and is now inside the phagocyte.
5. Phagosome Maturation: The newly formed phagosome undergoes a series of maturation steps
to fuse with other intracellular compartments, such as endosomes and lysosomes. This fusion
forms a phagolysosome, where the internalized particle is exposed to a variety of antimicrobial
components, including enzymes, reactive oxygen species (ROS), and acidic pH.
6. Microbial Killing: Within the phagolysosome, the foreign particle is subjected to various
mechanisms of destruction. Enzymes, such as proteases and nucleases, break down proteins and
nucleic acids, respectively. ROS generated by the phagocyte's NADPH oxidase system can also
destroy pathogens through oxidative damage. Acidic pH further enhances the activity of these
antimicrobial components.
7. Digestion and Excretion: Once the foreign particle is degraded and killed within the
phagolysosome, the resulting debris, including microbial remnants and cellular debris, is
gradually processed. The phagolysosome may undergo exocytosis, releasing the residual
material outside the cell, or the debris may be further processed for antigen presentation to
activate adaptive immune responses.

The molecular mechanism of phagocytosis involves a complex interplay of various receptors, signaling
pathways, cytoskeletal rearrangements, and intracellular trafficking events. This process is crucial for the
clearance of pathogens and the maintenance of immune homeostasis in the body.

2. Cells and Organs Involved in Immune Responses(SS): lymphocytes (T-cells, B cells, NK cells), mononuclear phagocytes, polymorphonuclear granulocytes, mast
cells, platelets, antigen presenting cell, primary and secondary clonal expansion of lymphocytes

6. Write down the components involved in different defense lines .

The body's defense system has two main lines of defense: the innate immune system and the adaptive
immune system.

The innate immune system is the body's first line of defense against infection. It is made up of physical
barriers, such as the skin and mucous membranes, as well as chemical defenses, such as stomach acid
and white blood cells.

The adaptive immune system is the body's second line of defense against infection. It is made up of cells
that can recognize specific invaders and produce antibodies to fight them off.
The components involved in different defense lines are as follows:

**Innate Immune System**

1. Physical barriers: The skin is the body's largest physical barrier. It is a tough, waterproof layer
that helps to prevent bacteria and viruses from entering the body. The mucous membranes that
line the respiratory, digestive, and reproductive tracts also act as physical barriers.
2. Chemical defenses: The body produces a number of chemical defenses that help to kill bacteria
and viruses. These include stomach acid, lysozyme, and complement proteins.
3. White blood cells: White blood cells are the body's main defense against infection. There are two
main types of white blood cells: phagocytes and lymphocytes. Phagocytes engulf and destroy
bacteria and viruses. Lymphocytes produce antibodies, which help to fight infection.

**Adaptive Immune System**

1. Lymphocytes: Lymphocytes are the cells of the adaptive immune system. There are two main
types of lymphocytes: B cells and T cells. B cells produce antibodies, which help to fight
infection. T cells help to regulate the immune response and to kill infected cells.
2. Antibodies: Antibodies are proteins that bind to specific antigens. Antigens are molecules that
are found on the surface of bacteria, viruses, and other foreign invaders. When an antibody
binds to an antigen, it triggers a series of events that lead to the destruction of the invader.
3. Memory cells: Memory cells are a type of lymphocyte that remembers specific invaders. When
the body is exposed to the same invader again, the memory cells can quickly produce antibodies
to fight it off.

The body's defense system is a complex and dynamic system that is constantly working to protect the
body from infection. By understanding how the immune system works, we can develop better ways to
prevent and treat disease.

7. " Natural killer cell recognizes infected and stressed cells and responds by killing these cells .
" - Explain this statement.
Natural killer cells (NK cells) are a type of lymphocyte that are part of the innate immune
system. They are able to recognize and kill cells that are infected with viruses or that are strssed.

NK cells do not need to be exposed to the specific virus or stressor in order to kill the infected or
stressed cell. This is because they recognize certain molecules that are common to all infected
or stressed cells.
When an NK cell recognizes an infected or stressed cell, it releases a number of proteins that kill
the cell. These proteins include perforins and granzymes. Perforins are proteins that create
holes in the cell membrane, while granzymes are proteins that kill the cell once it has been
damaged.
###NK cells play an important role in protecting the body from infection. They are able to kill
infected cells before the virus can replicate and cause disease. NK cells also play a role in tumor
surveillance. They can kill tumor cells that have escaped the body's other immune defenses.
NK cells are a valuable part of the immune system. They are able to quickly and efficiently kill
infected and stressed cells, which helps to protect the body from disease.
Here are some additional details about NK cells:
1. NK cells are found in the blood, lymph nodes, spleen, and other tissues.
2. NK cells are produced in the bone marrow.
3. NK cells mature in the thymus.
4. NK cells are able to recognize cells that are infected with viruses or that are stressed.
5. NK cells kill infected or stressed cells by releasing proteins that damage the cell
membrane or that kill the cell directly.
6. NK cells play an important role in protecting the body from infection and cancer.
8 . Discuss in breif the mechanism of clonal expansion 3.

Clonal expansion is the process by which a small number of lymphocytes (immune cells) that recognize a
specific antigen are rapidly multiplied to produce a large number of cells that are all specific for that
antigen. This process is essential for the adaptive immune system to mount an effective response to
infection.

Clonal expansion is triggered by the binding of the antigen to the specific receptor on the surface of the
lymphocyte. This binding event activates the lymphocyte, which then begins to divide rapidly. The
daughter cells are all identical to the parent cell, and they all have the same antigen receptor. This
process of rapid cell division can produce a large number of cells in a very short period of time.

The expanded clone of cells then differentiate into effector cells and memory cells. Effector cells are
responsible for mounting the immediate immune response to the infection. Memory cells are long-lived
cells that can quickly respond to a subsequent infection with the same antigen.

Clonal expansion is a critical process that allows the adaptive immune system to mount an effective
response to infection. By rapidly producing a large number of cells that are all specific for the invading
pathogen, the immune system can quickly overwhelm the pathogen and clear the infection.

Here are some of the key steps involved in clonal expansion:

1. **Antigen binding:** The first step in clonal expansion is the binding of the antigen to the
specific receptor on the surface of the lymphocyte. This binding event activates the lymphocyte.
2. **Cell division:** The activated lymphocyte then begins to divide rapidly. The daughter cells are
all identical to the parent cell, and they all have the same antigen receptor.
3. **Differentiation:** The expanded clone of cells then differentiates into effector cells and
memory cells. Effector cells are responsible for mounting the immediate immune response to
the infection. Memory cells are long-lived cells that can quickly respond to a subsequent
infection with the same antigen.
Clonal expansion is a complex process that is regulated by a number of factors, including the type of
antigen, the strength of the immune response, and the overall health of the individual.

3.The Humoral Immune Response(SM): Antigen-antibody interactions, affinity and avidity; antibodies, classification, structure, function and mechanism of action; interferons and their
functions.

8. What do you mean by herd immunity ?

Herd immunity is a community-level phenomenon that occurs when a large proportion of the population
is immune to a disease, making it difficult for the disease to spread. This can be achieved through
vaccination or through natural infection and recovery.

Herd immunity is important because it protects people who are unable to be vaccinated, such as infants
and people with certain medical conditions. It also helps to protect the community as a whole by
reducing the overall number of cases of disease.

The level of immunity needed to achieve herd immunity varies depending on the disease. For example,
herd immunity for measles is estimated to be around 90%, while herd immunity for chickenpox is around
80%.

There are a number of factors that can affect herd immunity, including the transmissibility of the disease,
the effectiveness of the vaccine, and the level of vaccination coverage in the community.

Herd immunity is a valuable tool for protecting communities from disease. By vaccinating or otherwise
protecting a large proportion of the population, we can help to keep everyone safe.

Here are some additional details about herd immunity:

1. Herd immunity is also known as community immunity or population immunity.

2. Herd immunity is a concept in epidemiology that describes how the spread of a disease can be
slowed or stopped by having a high proportion of the population immune to the disease.
3. Herd immunity can be achieved through vaccination, natural infection, or a combination of both.
4. The level of immunity needed to achieve herd immunity varies depending on the disease.
5. Herd immunity is a valuable tool for protecting communities from disease.

Overall, herd immunity is a valuable tool for protecting communities from disease. However, it is
important to note that herd immunity is not a perfect solution and that it can be difficult to achieve and
maintain.

9. Define pegasys ? Briefly describe the general action of interferons .

Pegasys is a brand name for a medication called peginterferon alfa-2a. It is a type of medication known
as an interferon, specifically a pegylated interferon. Pegasys is used for the treatment of certain viral
infections, such as chronic hepatitis B and hepatitis C.

Interferons, including peginterferon alfa-2a, are a group of signaling proteins that are naturally produced
by cells in response to viral infections, tumors, or other immune challenges. They play a crucial role in
the immune response and have various general actions:
 1. Antiviral Activity: Interferons can inhibit viral replication within infected cells. They stimulate the
production of enzymes that interfere with viral protein synthesis and replication, making it more
difficult for viruses to spread within the body.
2. Immunomodulation: Interferons help regulate and modulate the immune response. They
enhance the activity of immune cells, such as natural killer (NK) cells, macrophages, and
cytotoxic T cells, which are responsible for recognizing and eliminating infected or abnormal
cells. Interferons also influence the production and function of other immune system molecules.
3. Anti-proliferative Effects: Interferons can inhibit the growth and division of cells, including cancer
cells. They interfere with cell cycle progression and induce apoptosis (programmed cell death) in
certain types of cells, which can be beneficial in the treatment of certain cancers.
4. Immunostimulatory Effects: Interferons stimulate the immune system by promoting the
maturation and activation of dendritic cells, which are critical for initiating and coordinating
immune responses. They also enhance the expression of major histocompatibility complex
(MHC) molecules, facilitating antigen presentation and activation of T cells.

Pegylation, as in the case of peginterferon alfa-2a (Pegasys), involves attaching a polyethylene glycol
(PEG) molecule to the interferon. This modification extends the half-life of the interferon in the body,
allowing for less frequent dosing and improved pharmacokinetics.

Pegasys (peginterferon alfa-2a) is commonly used in combination with other antiviral medications for the
treatment of chronic hepatitis B and hepatitis C. By harnessing the general actions of interferons,
Pegasys helps suppress viral replication, modulate the immune response, and potentially achieve
sustained virologic response (SVR) in individuals with these viral infections.

10 . Describe the fragments of an immunoglobulin treated with pepsin and papain .

Here is a table that summarizes the fragments of immunoglobulins that are generated by pepsin and
papain:

Enzyme Fragments

Pepsin Fab fragments, Fc fragment

Papain Fab fragments, Fc fragments, smaller fragments

When an immunoglobulin (antibody) is treated with pepsin or papain, it undergoes enzymatic digestion
resulting in the generation of specific fragments. Here's a description of the fragments produced by
treating immunoglobulins with pepsin and papain:

1. Pepsin Digestion:

Pepsin is an enzyme that cleaves immunoglobulins specifically at the hinge region, which is a flexible
region that connects the two heavy chains of an antibody. The digestion with pepsin yields two main
fragments:
 i. Fab Fragments: Pepsin cleaves the antibody near the hinge region, resulting in
the production of two identical antigen-binding fragments known as Fab
(Fragment antigen-binding). Each Fab fragment consists of one complete light
chain and the variable domain of one heavy chain. Fab fragments retain the
ability to bind to antigens.

ii. Fc Fragment: The remaining portion of the antibody after pepsin digestion is
called the Fc (Fragment crystallizable) fragment. It consists of the constant
domains of the heavy chains and is responsible for effector functions, such as
binding to Fc receptors on immune cells and activating complement.

2. Papain Digestion:

Papain is another enzyme commonly used to cleave immunoglobulins. Papain digestion produces three
main fragments:

i. Fab Fragments: Similar to pepsin digestion, papain cleaves the antibody near the
hinge region, resulting in the generation of Fab fragments. These Fab fragments
retain antigen-binding activity.

ii. Fc Fragment: Papain digestion cleaves the antibody just below the hinge region,
resulting in the separation of the Fc fragment. The Fc fragment contains the
constant domains of the heavy chains, responsible for effector functions.

iii. F(ab')2 Fragment: Papain digestion also produces an additional fragment known
as F(ab')2. This fragment consists of two antigen-binding fragments (Fab') linked
together by disulfide bonds. The F(ab')2 fragment lacks the Fc region and cannot
bind to Fc receptors or activate complement.

The specific fragments generated by pepsin and papain digestion allow for the separation of the antigen-
binding regions (Fab) from the effector regions (Fc) of immunoglobulins. This enables researchers to
study and utilize these fragments for various applications, such as antigen detection,
immunohistochemistry, and therapeutic antibody engineering.

11. What is phagocyte ? Describe the mechanism of phagocytes activation .

A phagocyte is a type of immune cell that specializes in phagocytosis, the process of engulfing and
digesting foreign particles, such as bacteria, cellular debris, and other pathogens. Phagocytes play a
critical role in the innate immune response, acting as the first line of defense against invading
microorganisms. The two main types of phagocytes are neutrophils and macrophages.

Mechanism of Phagocyte Activation:

1. Chemotaxis: The activation of phagocytes begins with the detection of chemical signals called
chemoattractants. These signals are released by injured tissues, microbial products, or immune
cells in response to infection or inflammation. Phagocytes detect these chemoattractants and
migrate towards the site of infection through a process known as chemotaxis.
2. Receptor-Mediated Recognition: Phagocytes have surface receptors called pattern recognition
receptors (PRRs) that can recognize specific molecules known as pathogen-associated molecular
patterns (PAMPs). PAMPs are present on the surface of pathogens and are not found on host
cells. Binding of PAMPs to PRRs triggers the activation of phagocytes.
3. Opsonization: Opsonization is the process of tagging pathogens for recognition and engulfment
by phagocytes. Opsonins, such as antibodies or complement proteins, bind to the surface of
pathogens, marking them for recognition by phagocytes. Opsonins enhance phagocytosis by
promoting the attachment of the phagocyte to the opsonized pathogen.
4. Engulfment: Once a phagocyte recognizes a pathogen, it extends pseudopods (temporary
projections of the cell membrane) around the target, enclosing it in a phagocytic cup. The
pseudopods fuse together, forming a phagosome, which is a membrane-bound vesicle
containing the engulfed particle.
5. Phagosome Maturation: The phagosome undergoes a series of maturation steps. It fuses with
intracellular compartments, such as endosomes and lysosomes, forming a phagolysosome. This
fusion delivers enzymes, reactive oxygen species (ROS), and acidic pH to the phagolysosome,
creating a hostile environment for the pathogen.
6. Microbial Killing and Digestion: Within the phagolysosome, the pathogen is exposed to a variety
of antimicrobial mechanisms. These include the activity of lysosomal enzymes that degrade
proteins, nucleic acids, and carbohydrates, as well as the production of ROS that generate toxic
reactive molecules. These processes lead to the destruction and digestion of the engulfed
pathogen.
7. Exocytosis or Antigen Presentation: After the pathogen is killed and digested, the remnants are
either eliminated from the phagocyte through exocytosis or processed for antigen presentation.
Antigen presentation involves breaking down the pathogen's components into smaller fragments
and presenting them on the phagocyte's surface using major histocompatibility complex (MHC)
molecules. This allows the phagocyte to present antigens to other immune cells, initiating
adaptive immune responses.

Phagocyte activation is a tightly regulated process that involves the coordination of various receptors,
signaling pathways, and intracellular mechanisms. This process is crucial for the clearance of pathogens
and the maintenance of immune homeostasis in the body.

12. Write short note on transcystasis

Transcytosis is a type of endocytosis in which a cell takes in a particle or molecule on one side of its
membrane and then transports it across the cell to the other side, releasing it into the extracellular
space. This process is important for the transport of molecules across the blood-brain barrier, as well as
for the transport of immune cells and other particles across the walls of capillaries and other tissues.
###

Transcytosis is initiated when a particle or molecule binds to a receptor on the cell surface. The receptor
then triggers a series of events that lead to the formation of a vesicle around the particle or molecule.
The vesicle is then transported across the cell by the cytoskeleton, and it eventually fuses with the cell
membrane on the other side, releasing the particle or molecule into the extracellular space.

Transcytosis is a complex process that is regulated by a number of factors, including the type of particle
or molecule being transported, the type of cell involved, and the environment in which the cell is located
###.

Here are some of the key steps involved in transcytosis:

1. Binding of the particle or molecule to a receptor on the cell surface.

2. Formation of a vesicle around the particle or molecule.
3. Transport of the vesicle across the cell by the cytoskeleton.
4. Fusion of the vesicle with the cell membrane on the other side.
5. Release of the particle or molecule into the extracellular space.

Transcytosis is a vital process that allows cells to transport molecules and particles across their
membranes. It is essential for a variety of cellular functions, including the transport of immune cells, the
transport of nutrients and hormones, and the transport of waste products.

13. Define trancystosis . How opsonizaton is promted by antibody

**Opsonization** is the process by which antibodies coat foreign particles, making them more easily
recognized and destroyed by phagocytes. Opsonization is an important part of the body's immune
system. It helps to protect the body from infection by making it easier for phagocytes to destroy foreign
particles.

Antibodies bind to specific antigens on the surface of foreign particles. When an antibody binds to an
antigen, it changes the shape of the antigen. This change in shape makes the antigen more easily
recognized by phagocytes. Phagocytes have receptors on their surface that bind to antibodies. When a
phagocyte binds to an antibody-coated foreign particle, it engulfs the particle and destroys it.

Opsonization is a critical part of the body's immune system. It helps to protect the body from infection
by making it easier for phagocytes to destroy foreign particles.

Here are some of the ways that antibodies promote opsonization:

1. Antibodies can bind to antigens on the surface of foreign particles, making them more visible to
phagocytes.
2. Antibodies can coat foreign particles, making them more sticky and easier for phagocytes to
engulf.
3. Antibodies can activate complement proteins, which can damage foreign particles and make
them easier for phagocytes to destroy.
Overall, opsonization is an important part of the body's immune system. It helps to protect the body
from infection by making it easier for phagocytes to destroy foreign particles.

14. Briefly describe the general mode of action of interferon .

Interferons are a group of proteins that are produced by cells in response to infection. They have a
variety of effects on cells, including:

1. **Inhibiting viral replication:** Interferons can interfere with the ability of viruses to
replicate by blocking their ability to enter cells, transcribe their genes, or translate their
proteins.
2. **Amplifying the immune response:** Interferons can amplify the immune response by
activating other immune cells, such as natural killer cells and T cells.
3. **Protecting cells from damage:** Interferons can protect cells from damage by
suppressing inflammation and promoting cell repair.

Interferons are generally well-tolerated, but they can cause some serious side effects, such as bone
marrow suppression and liver damage. If you are considering interferon therapy, talk to your doctor
about the risks and benefits.

Here are some additional details about interferons:

1. Interferons are produced by a variety of cells, including white blood cells, fibroblasts,
and epithelial cells.
2. Interferons are released in response to infection with viruses, bacteria, and parasites.
3. Interferons are also released in response to stress, injury, and inflammation.
4. Interferons are a family of proteins that are structurally and functionally related.
5. There are three main types of interferons: alpha, beta, and gamma.
6. Interferons are used to treat a variety of diseases, including hepatitis B and C, cancer,
and multiple sclerosis.

Interferons are an important part of the body's immune system. They help to protect the body from
infection by interfering with the ability of viruses to replicate and by amplifying the immune response.

15. Explain the therapeute uses of immunotoxins composed of monoclonal antibody with an example .

‘’’

Immunotoxins are a class of therapeutic agents designed to selectively target and destroy specific cells in
the body, typically cancer cells. They are composed of two main components: a targeting component
and a toxic component.

Immunotoxins are therapeutic agents that combine the specific targeting ability of monoclonal
antibodies (mAbs) with the potent cytotoxic effects of toxins. They are designed to selectively deliver
toxins to target cells expressing specific antigens, thereby providing a targeted approach for treating
various diseases. Here's an explanation of the therapeutic uses of immunotoxins, along with an example:
Therapeutic Uses of Immunotoxins:

1. Cancer Treatment: Immunotoxins have been extensively studied and developed as potential
treatments for cancer. They can be designed to target antigens that are overexpressed on cancer
cells while sparing normal cells. When the immunotoxin binds to the cancer cell, it is
internalized, and the toxin component induces cell death, leading to the destruction of cancer
cells. This targeted approach minimizes the toxicity to healthy tissues compared to conventional
chemotherapy.
2. Autoimmune Disorders: Immunotoxins can also be used in the treatment of autoimmune
disorders, where the immune system mistakenly attacks healthy tissues. By targeting and
eliminating specific cells involved in the autoimmune response, immunotoxins can help
modulate the immune response and reduce the damage to the affected tissues.
3. Infectious Diseases: Immunotoxins can be utilized to target and eliminate specific pathogens or
infected cells. By delivering toxins directly to the infectious agent or the host cells it invades,
immunotoxins can effectively kill the pathogens or reduce their replication, contributing to the
control of infectious diseases.

Example of an Immunotoxin: One example of an immunotoxin is Brentuximab vedotin (trade name:

Adcetris). Brentuximab vedotin is composed of an anti-CD30 monoclonal antibody conjugated to a
potent cytotoxic agent called monomethyl auristatin E (MMAE). CD30 is a protein expressed on the
surface of certain lymphomas and other malignancies. When Brentuximab vedotin binds to CD30-
expressing cancer cells, it is internalized, and MMAE is released inside the cell. MMAE disrupts the
microtubule network, causing cell cycle arrest and inducing cell death specifically in CD30-positive cancer
cells.

Brentuximab vedotin has been approved for the treatment of certain types of lymphomas, such as
Hodgkin lymphoma and anaplastic large cell lymphoma, where CD30 is overexpressed. It has shown
significant clinical efficacy, demonstrating the therapeutic potential of immunotoxins in the targeted
treatment of cancer.

It's important to note that the development and use of immunotoxins require careful consideration of
factors such as target selection, toxicity profiles, and dosing strategies to maximize efficacy while
minimizing side effects.

4. The cell-mediated Immune Response(SS): Recognition of antigen by T cells, antigen presentation, the major histocompatibility complexes or MHC molecules, the role of
cytokines and the regulation of immune responses.

16. Define cell mediated immune response . Briefly discuss the classifications and functions of T -
lymphocytes .

The cell-mediated immune response is a specific immune response carried out by immune cells,
particularly T cells, to combat intracellular pathogens and eliminate infected cells.

The cell-mediated immune response is a type of immune response involving T lymphocytes. It targets
infected or abnormal cells and is initiated by antigen-presenting cells presenting antigens on MHC
molecules. T cells recognize these antigens and coordinate immune responses, including direct killing of
infected cells by cytotoxic T cells and regulation of immune reactions by regulatory T cells.
T lymphocytes, or T cells, are a type of white blood cell that play a major role in the body's adaptive
immune system. They are produced in the thymus gland and circulate throughout the body, where they
can recognize and respond to specific antigens.

T cells are classified into two main groups: helper T cells (Th cells) and cytotoxic T cells (Tc cells).

Helper T cells (Th cells: help to activate other immune cells, such as B cells and macrophages. They also
produce cytokines, which are proteins that help to regulate the immune response. There are two main
types of Th cells: Th1 cells and Th2 cells.

a. **Th1 cells** help to fight against intracellular pathogens, such as viruses and
bacteria. They do this by activating macrophages and other immune cells to kill
infected cells.
b. **Th2 cells** help to fight against extracellular pathogens, such as parasites.
They do this by activating B cells to produce antibodies that can bind to and
destroy the pathogens.

Cytotoxic T cells (Tc cells): kill cells that are infected with viruses or bacteria, or that have become
cancerous. They do this by releasing proteins called perforins and granzymes, which damage the cell
membrane and cause the cell to die.

In addition to Th cells and Tc cells, there are a number of other types of T cells, including:

1. **Regulatory T cells (Treg cells)** help to suppress the immune response. They do this by
releasing proteins that inhibit the activity of other immune cells. Treg cells are important for
preventing autoimmune diseases, which are diseases in which the immune system attacks
healthy cells.
2. **Natural killer T cells (NKT cells)** are a type of T cell that can kill cells that are infected with
viruses or bacteria, or that have become cancerous. They do this by releasing proteins called
perforins and granzymes, which damage the cell membrane and cause the cell to die.
3. **γδ T cells** are a type of T cell that express a different type of T-cell receptor than other T
cells. They are found in the skin and gut, where they help to protect against infection.

T cells play a vital role in the body's immune system. They help to protect the body from infection,
cancer, and autoimmune diseases.

T cells, or T lymphocytes, are a type of white blood cell that play a major role in the body's adaptive
immune system. They are produced in the thymus gland and circulate throughout the body, where they
can recognize and respond to specific antigens.

T cells have a variety of functions, including:

1. **Helping other immune cells:** T cells help to activate other immune cells, such as B
cells and macrophages. They do this by releasing proteins called cytokines, which help to
regulate the immune response.
 2. **Killing infected cells:** T cells can kill cells that are infected with viruses or bacteria, or
that have become cancerous. They do this by releasing proteins called perforins and
granzymes, which damage the cell membrane and cause the cell to die.
3. **Regulating the immune response:** T cells can help to suppress the immune
response. They do this by releasing proteins that inhibit the activity of other immune
cells. This is important for preventing autoimmune diseases, which are diseases in which
the immune system attacks healthy cells.
4. **Providing memory:** T cells can remember specific antigens, which allows them to
mount a faster and more effective immune response if the body is exposed to the same
antigen again.

T cells play a vital role in the body's immune system. They help to protect the body from infection,
cancer, and autoimmune diseases.

17 . What is co - stimulation ?

Co-stimulation refers to the additional signals required for full activation of T cells during an immune
response. It involves the interaction between co-stimulatory molecules on antigen-presenting cells and
their receptors on T cells. Co-stimulation enhances T cell activation, ensures specificity, regulates
immune responses, and helps prevent tolerance to self-antigens.

18. What is co - stimulatory factor

A co-stimulatory factor is a molecule that binds to a receptor on a T cell and helps to activate the T cell.
Co-stimulatory factors are important for the development of an effective immune response.

There are two main types of co-stimulatory factors: B7 molecules and CD40 ligand. B7 molecules are
expressed on antigen-presenting cells and bind to receptors on T cells. The most important B7 molecule
is B7-1, which binds to the CD28 receptor on T cells. CD40 ligand is expressed on activated T cells and
binds to CD40 on antigen-presenting cells. CD40 ligand binding activates antigen-presenting cells, which
in turn produce more co-stimulatory molecules and cytokines.

Co-stimulatory factors are essential for the activation of T cells. Without co-stimulation, T cells will not
be activated and will not be able to mount an immune response. Co-stimulation is also important for the
development of tolerance. Tolerance is the ability of the immune system to ignore harmless antigens.
Without co-stimulation, T cells that recognize harmless antigens would be activated and could mount an
immune response against those antigens.

Co-stimulation is a complex process that is essential for the proper functioning of the immune system. By
understanding co-stimulation, scientists are able to develop new treatments for diseases such as cancer
and autoimmune disorders.

Here are some examples of co-stimulatory factors:

1. B7-1
2. B7-2
3. CD80
 4. CD86
5. CD40
6. CD40 ligand

These molecules are expressed on different types of cells, including antigen-presenting cells, T cells, and
B cells. They play a role in the activation of T cells and the development of an immune response.

18.1 Discuss in brief the mechanison of co stimulation 4.

Sure. Here is a brief overview of the mechanism of co-stimulation:

1. **Antigen recognition:** The first step in T cell activation is the recognition of an

antigen by the T cell receptor (TCR). The TCR is a protein on the surface of T cells that
binds to specific antigens.
2. **Co-stimulatory signal:** The second step in T cell activation is the receipt of a co-
stimulatory signal. Co-stimulatory signals are provided by molecules on antigen-
presenting cells (APCs) that bind to receptors on T cells.
3. **Signal transduction:** The binding of co-stimulatory molecules to receptors on T cells
triggers a cascade of signaling events inside the T cell. These signaling events lead to the
activation of T cells.
4. **T cell proliferation and differentiation:** Activated T cells proliferate and differentiate
into effector T cells. Effector T cells are responsible for mounting an immune response
against the antigen that they recognize.

Co-stimulation is a critical step in T cell activation. Without co-stimulation, T cells will not be activated
and will not be able to mount an immune response.

Here are some additional details about the mechanism of co-stimulation:

a. **B7 molecules:** B7 molecules are expressed on APCs and bind to receptors on T cells.
The most important B7 molecule is B7-1, which binds to the CD28 receptor on T cells.
b. **CD40 ligand:** CD40 ligand is expressed on activated T cells and binds to CD40 on
APCs. CD40 ligand binding activates APCs, which in turn produce more co-stimulatory
molecules and cytokines.
c. **Signal transduction:** The binding of co-stimulatory molecules to receptors on T cells
triggers a cascade of signaling events inside the T cell. These signaling events lead to the
activation of T cells.
d. **T cell proliferation and differentiation:** Activated T cells proliferate and differentiate
into effector T cells. Effector T cells are responsible for mounting an immune response
against the antigen that they recognize.

Co-stimulation is a complex process that is essential for the proper functioning of the immune system. By
understanding co-stimulation, scientists are able to develop new treatments for diseases such as cancer
and autoimmune disorders.
19. What is cytokines ? Illustrate how cytokines control immune responses provided by lymphocytes.

Cytokines are small proteins that act as messengers between cells of the immune system. They are
produced by a variety of cells, including lymphocytes, macrophages, and dendritic cells. Cytokines play a
role in many aspects of the immune response, including:

1. Inflammation: Cytokines help to recruit immune cells to the site of an infection or injury. They
also help to activate these cells and promote the production of antibodies and other immune
molecules.
2. Cell growth and differentiation: Cytokines help to regulate the growth and differentiation of
immune cells. They also help to control the production of new immune cells.
3. Apoptosis: Cytokines can also induce apoptosis, or programmed cell death, in immune cells. This
helps to remove damaged or infected cells from the body.

Cytokines can have both positive and negative effects on the immune response. Too much of a particular
cytokine can lead to an overactive immune response, which can cause inflammation and damage to
healthy tissue. Too little of a particular cytokine can lead to an underactive immune response, which can
make it difficult for the body to fight infection.

Cytokines can also interact with each other to produce different effects. For example, some cytokines
can enhance the effects of other cytokines, while others can suppress them. This complex interplay of
cytokines helps to coordinate the immune response and ensure that it is effective in fighting infection.

5. Complements(SM): Activities of complement proteins, activation of complement, classical pathway, regulation of classical pathway activation, alternative pathway, activation and amplification loop,
their regulation, membrane attack complex, biological effects of complement.

20. What do you mean by complement ?

The complement system (CS) is a group of proteins in the blood that help the body fight infection. It does
this by:

1. Opsonizing pathogens: This means coating pathogens with proteins that make them easier for
phagocytes (white blood cells that eat germs) to engulf and destroy.
2. Lysing pathogens: This means creating holes in the membranes of pathogens, which kills them.
 3. Promoting inflammation: This attracts more immune cells to the site of infection, which helps to
fight the infection more effectively.
4. Regulating the immune response: The CS can also help to regulate the immune response,
preventing it from becoming too strong and causing damage to healthy tissue.

The CS is made up of more than 30 proteins that circulate in the blood in an inactive form. When the CS
is activated, it triggers a cascade of reactions that produce proteins that can damage pathogens or help
to fight infection in other ways.

21. Complement system completes the action of antibody---justify2

The complement system plays a crucial role in the immune response and works in coordination with
antibodies to enhance their effectiveness in combating pathogens. Here are several ways in which the
complement system complements the action of antibodies:

1. Enhancing Antibody-Mediated Opsonization: Antibodies can mark pathogens for destruction by

a process called opsonization. The complement system enhances this process by binding to the
antibodies attached to the pathogen's surface and promoting the recruitment and activation of
phagocytic cells, such as macrophages and neutrophils. This facilitates the efficient engulfment
and elimination of the opsonized pathogen.
2. Promoting Direct Pathogen Lysis: The complement system can directly lyse pathogens through a
process called the membrane attack complex (MAC) formation. Antibodies, when bound to
pathogens, can activate the complement system through the classical pathway. This leads to the
assembly of MAC, resulting in the formation of pores in the pathogen's membrane and causing
its lysis or destruction.
3. Amplifying Inflammatory Response: Antibodies, upon binding to pathogens or antigens, can
activate the complement system through the classical pathway. This activation triggers the
release of inflammatory mediators, such as histamine and cytokines, which attract immune cells
to the site of infection or inflammation. This amplifies the immune response and promotes the
recruitment and activation of other immune cells to eliminate the pathogen.
4. Clearing Immune Complexes: Immune complexes are formed when antibodies bind to antigens,
such as toxins or foreign proteins. The complement system, particularly the classical pathway,
can recognize and bind to these immune complexes. This promotes their clearance by enhancing
phagocytosis or facilitating their removal by other components of the immune system,
preventing potential tissue damage caused by the deposition of immune complexes.
5. Modulating Adaptive Immune Responses: The complement system can interact with antibodies
to modulate the adaptive immune response. For example, complement fragments can act as co-
stimulatory signals for B cells, promoting their activation, proliferation, and antibody production.
Additionally, the complement system can participate in antigen presentation, assisting in the
processing and presentation of antigens to T cells.

In summary, the complement system complements the action of antibodies by enhancing opsonization,
promoting direct pathogen lysis, amplifying the inflammatory response, clearing immune complexes,
and modulating adaptive immune responses. These interactions between the complement system and
antibodies lead to a more effective and coordinated immune response against pathogens.
22. Write down the basic functions of complement system .

The complement system is a vital part of the immune system and performs several essential functions:

1. Pathogen Recognition: The complement system recognizes and distinguishes foreign pathogens,
such as bacteria, viruses, and fungi, from host cells. It can detect specific molecular patterns on
the surface of pathogens or immune complexes formed by the binding of antibodies to
pathogens.
2. Opsonization: The complement system promotes opsonization, which is the process of marking
pathogens for phagocytosis. It coats the surface of pathogens with complement proteins, such
as C3b, making them more recognizable to phagocytic cells, such as macrophages and
neutrophils. This enhances the uptake and elimination of the pathogens.
3. Inflammation Induction: The complement system triggers and amplifies inflammatory responses.
It releases various inflammatory mediators, including histamine and cytokines, which attract
immune cells to the site of infection or inflammation. This leads to increased blood flow,
vasodilation, and recruitment of immune cells to combat the pathogens.
4. Membrane Attack Complex (MAC) Formation: The complement system can directly lyse certain
pathogens through the formation of a membrane attack complex (MAC). This complex, formed
by the sequential assembly of complement proteins, creates pores in the pathogen's membrane,
disrupting its integrity and leading to cell lysis.
5. Clearance of Immune Complexes: The complement system plays a role in the clearance of
immune complexes formed by the binding of antibodies to pathogens or soluble antigens. It
recognizes and binds to these immune complexes, facilitating their removal by phagocytic cells
or other mechanisms to prevent tissue damage.
6. Enhancement of Adaptive Immune Responses: The complement system interacts with
antibodies and assists in the activation and regulation of the adaptive immune response. It can
act as a co-stimulatory signal for B cells, promoting their activation and antibody production.
Additionally, complement proteins can participate in antigen presentation and assist in the
processing and presentation of antigens to T cells.

These functions collectively contribute to the complement system's role in pathogen detection,
elimination, inflammation, immune regulation, and immune complex clearance, making it a critical
component of the immune defense against infections and other threats to the body.

23. Mention the protein of the complement system .

The complement system is a group of proteins in the blood that help the body fight infection. It is made
up of more than 30 proteins that circulate in the blood in an inactive form. When the complement
system is activated, it triggers a cascade of reactions that produce proteins that can damage pathogens
or help to fight infection in other ways.

Here are some of the proteins of the complement system:

1. C1: C1 is a complex of proteins that is the first component of the classical pathway. It
is activated by antibodies binding to pathogens.
2. C2: C2 is a protein that is activated by C1. It forms a complex with C4 to create the
C3 convertase, which is responsible for cleaving C3.
 3. C3: C3 is the most abundant protein in the complement system. It is cleaved by the
C3 convertase to form C3a and C3b. C3a is an anaphylatoxin that can cause
inflammation. C3b can bind to pathogens and activate the alternative pathway.
4. C4: C4 is a protein that is activated by C1. It forms a complex with C2 to create the
C3 convertase, which is responsible for cleaving C3.
5. C5: C5 is a protein that is activated by the C3bBb complex. It forms a complex with
C6, C7, C8, and C9 to create the membrane attack complex (MAC), which can create
holes in the membranes of pathogens and kill them.

These are just a few of the many proteins that make up the complement system. The complement
system is a complex system that plays an important role in the immune system. It helps to fight infection
by opsonizing pathogens, lysing pathogens, promoting inflammation, and regulating the immune
response.

24. Describe the classical pathway for generation of C3 convertase.

The classical pathway is one of the three pathways that can activate the complement system. It is
primarily triggered by the binding of antibodies, particularly IgM or IgG subclasses, to their specific
targets, such as pathogens or immune complexes. The activation of the classical pathway leads to the
generation of the C3 convertase, which cleaves C3 into C3a and C3b, initiating downstream complement
cascade reactions.

Here is a step-by-step description of the classical pathway for the generation of the C3 convertase:
1. Antibody Binding: The classical pathway is initiated when antibodies, specifically IgM or IgG subclasses,
bind to their target antigen on a pathogen or immune complex. This binding can occur through the
variable regions of the antibody, recognizing specific antigenic determinants.
2. C1 Binding: Upon antibody binding, the first component of the complement system, C1, recognizes and
binds to the Fc region of the antibody that is bound to the antigen. C1 is a complex consisting of three
subcomponents: C1q, C1r, and C1s.
3. C1 Activation: The binding of C1q to antibody result in the activation of C1r which then turn activate C1s
The result is the formation of activated C1qrs which is an enzyme
4. C1s Activation of C4 and C2: Activated C1qrs then cleaves the complement 4 (C4) into C4a and C4b. C4b
covalently attaches to the target surface, while C4a is released in the microenvironment. The activated
C4b serves as an opsonin and promotes the recruitment of other complement proteins.
5. C4b Binding and C2 Cleavage: The C4b that has bound to the target surface can then interact with
complement component 2 (C2). C1qrs also cleaves C2 into C2a and C2b, generating a C4bC2a complex.
This complex is the C3 convertase of the classical pathway, also known as C4bC2a.
6. C3 Cleavage and C3 Convertase Formation: The C4bC2a complex acts as an enzyme and cleaves the
complement component 3 (C3) into two fragments: C3a and C3b. C3b covalently binds to the surface of
the pathogen or immune complex, contributing to opsonization and the formation of the C3 convertase.
7. C3 Convertase Amplification: The initial C4bC2a complex generated by the cleavage of C4 and C2 can also
interact with additional C3 molecules. This leads to the formation of a larger C3 convertase known as
C4bC2aC3b, which can further cleave C3 molecules, amplifying the complement cascade.

The generation of the C3 convertase in the classical pathway allows for the subsequent activation of
downstream components, leading to the formation of the membrane attack complex (MAC),
opsonization, and the recruitment of inflammatory cells. This coordinated response plays a crucial role in
eliminating pathogens and immune complexes and regulating immune responses.

25. Define complement system . Describe the lectin pathway of complement activation .

The complement system is a part of the immune system that consists of a series of proteins that can be
activated by various triggers, leading to a cascade of reactions that help to eliminate pathogens, promote
inflammation, and regulate immune responses.

The lectin pathway is one of the three pathways that can activate the complement system. It is initiated
by the binding of certain pattern-recognition molecules, called mannose-binding lectins (MBL), or
ficolins, to specific sugar molecules (mannose or N-acetylglucosamine) on the surface of pathogens. The
lectin pathway serves as a bridge between innate and adaptive immunity and plays a role in the
recognition and elimination of pathogens.

Here is a step-by-step description of the lectin pathway of complement activation:

1. Recognition Molecule Binding: Pattern-recognition molecules, such as MBL or ficolins, bind to

specific sugar molecules (mannose or N-acetylglucosamine) on the surface of pathogens. MBL is
primarily involved in the lectin pathway.
2. MASP Activation: Upon binding to the pathogen, MBL-associated serine proteases (MASPs),
particularly MASP-2, become activated. These serine proteases are associated with MBL and play
a role similar to C1r and C1s in the classical pathway.
3. Cleavage of Complement Components: Activated MASPs cleave complement components C4
and C2, similar to the classical pathway. Cleavage of C4 into C4a and C4b, followed by cleavage of
C2 into C2a and C2b, generates the C4bC2a complex, which acts as the C3 convertase.
4. C3 Cleavage and Amplification: The C4bC2a complex cleaves the complement component C3
into C3a and C3b, similar to the classical pathway. This leads to the formation of a larger C3
convertase, known as C4bC2aC3b. The amplification of the complement cascade continues,
promoting opsonization and downstream complement activation.
5. Activation of the Terminal Pathway: The lectin pathway, like other complement pathways,
eventually leads to the activation of the terminal pathway. C3b generated through the lectin
pathway can bind to C5, enabling the formation of the C5 convertase. This results in the
subsequent cleavage of C5 into C5a and C5b, initiating the assembly of the membrane attack
complex (MAC) and leading to cell lysis.

The lectin pathway of complement activation provides a mechanism for the recognition and elimination
of pathogens, particularly those with specific sugar structures on their surfaces. It operates in parallel
with the classical pathway and the alternative pathway, collectively contributing to an effective and
coordinated immune response against invading pathogens.

26. What are the most important biologically active products of complement activation .

The complement system activation generates several biologically active products that play important
roles in various immune processes. Here are some of the most significant biologically active products of
complement activation:
 1. C3a and C5a (Anaphylatoxins): C3a and C5a are small peptide fragments generated during
complement activation. They act as potent chemoattractants, recruiting immune cells, such as
neutrophils, eosinophils, and monocytes, to the site of complement activation. Additionally, they
induce the release of histamine from mast cells, promoting inflammation and vasodilation.
2. C3b and C4b (Opsonins): C3b and C4b are complement components that can bind to pathogens
or immune complexes, marking them for recognition and phagocytosis by cells possessing
complement receptors, such as macrophages and neutrophils. Opsonization enhances the
efficiency of phagocytosis and elimination of the targeted particles.
3. Membrane Attack Complex (MAC): The MAC is formed by the sequential assembly of
complement components C5b, C6, C7, C8, and multiple molecules of C9. It forms pores in the
membranes of target cells, leading to cell lysis and destruction. The MAC is crucial for eliminating
pathogens and infected cells.
4. C3a, C4a, and C5a (Anaphylatoxins): In addition to their chemotactic effects, C3a, C4a, and C5a
can also induce the release of inflammatory mediators, such as histamine, from mast cells. This
promotes vasodilation, increased vascular permeability, and the recruitment of immune cells,
contributing to the inflammatory response.
5. C5a (Immunomodulatory effects): C5a has diverse immunomodulatory effects. It can stimulate
the expression of adhesion molecules on endothelial cells, promoting the recruitment of
immune cells to the site of infection or inflammation. C5a can also enhance the activation and
proliferation of B cells, modulate T cell responses, and promote cytokine production.
6. Complement Receptors (CRs): Various cells express complement receptors, such as CR1, CR2,
and CR3, which bind to complement components or fragments. These interactions mediate
diverse functions, including phagocytosis, antigen presentation, modulation of B and T cell
responses, and clearance of immune complexes.

These biologically active products of complement activation collectively contribute to the immune
response by promoting inflammation, recruiting immune cells, enhancing phagocytosis, eliminating
pathogens, and modulating immune cell functions. They play essential roles in host defense, immune
regulation, and the maintenance of homeostasis.

27. Show how C3 convertase is produced in classical and alternative pathway of complement system .

Sure! I'll explain how the C3 convertase is produced in both the classical and alternative pathways of the
complement system:

1. Classical Pathway:

In the classical pathway, the C3 convertase is formed through a cascade of reactions triggered by the
binding of antibodies (IgM or IgG subclasses) to target antigens. Here's how it occurs:

i. Antibody Binding: Antibodies recognize and bind to specific antigens on the

surface of pathogens or immune complexes.
ii. C1 Complex Activation: Upon antibody binding, the complement component C1
binds to the Fc region of the antibody, leading to the activation of the C1
complex. The C1 complex consists of C1q, C1r, and C1s.
 iii. C4 and C2 Cleavage: Activated C1s cleaves the complement component C4 into
C4a and C4b. C4b then binds to the surface of the pathogen or immune
complex. Subsequently, C1s cleaves C2 into C2a and C2b.
iv. C3 Convertase Formation: The C4b fragment that has bound to the target
surface can then interact with C2a to form the C4bC2a complex. This complex
serves as the C3 convertase of the classical pathway.

v. C3 Cleavage and Amplification: The C4bC2a complex acts as an enzyme and

cleaves the complement component C3 into C3a and C3b. This cleavage
generates a larger C3 convertase, known as C4bC2aC3b, which can further
cleave C3 molecules, amplifying the complement cascade.

2. Alternative Pathway:

The alternative pathway can be initiated spontaneously, without the presence of antibodies. It involves
the recognition of certain molecular patterns on the surface of pathogens. Here's how the C3 convertase
is formed in the alternative pathway:

i. Spontaneous C3 Hydrolysis: In the absence of external triggers, a small fraction

of the complement component C3 spontaneously hydrolyzes into C3(H2O),
which undergoes conformational changes.
ii. C3 Binding and Stabilization: The conformationally altered C3(H2O) binds to
nearby complement factor B (CFB). This binding facilitates the cleavage of CFB
by complement factor D (CFD), resulting in the formation of C3(H2O)Bb
complex.
iii. C3 Convertase Formation: The C3(H2O)Bb complex acts as the C3 convertase of
the alternative pathway. It cleaves C3 into C3a and C3b, generating more C3
convertase molecules.
iv. C3 Amplification and Positive Feedback: The newly formed C3b can bind to the
C3 convertase (C3(H2O)Bb), forming C3bBb. This complex serves as an
amplification loop, leading to the production of additional C3b and C3
convertase molecules.

It's important to note that in both pathways, the C3 convertase (C4bC2a in the classical pathway and
C3(H2O)Bb in the alternative pathway) cleaves C3 into C3a and C3b, initiating downstream complement
cascade reactions and amplifying the immune response.

28. What is anaphylatoxin ?Write down the biological effects of C5a***

Anaphylatoxins are small peptide fragments that are generated during complement system activation,
specifically through the cleavage of complement components C3 and C5. These fragments, including C3a,
C4a, and C5a, have potent biological effects on various immune cells and contribute to the inflammatory
response.
C5a, in particular, is a highly potent anaphylatoxin with diverse biological effects. Here are some of the
biological effects of C5a:

1. Chemotaxis: C5a acts as a potent chemoattractant, attracting and recruiting immune cells to the
site of inflammation or infection. It attracts neutrophils, monocytes, eosinophils, and mast cells,
facilitating their migration to the site of complement activation.
2. Leukocyte Activation: C5a activates and enhances the functions of leukocytes. It induces the
expression of adhesion molecules on endothelial cells, facilitating the attachment and migration
of leukocytes across blood vessel walls. C5a also stimulates the release of pro-inflammatory
cytokines and chemokines by leukocytes, amplifying the inflammatory response.
3. Mast Cell Activation: C5a triggers the release of histamine and other inflammatory mediators
from mast cells. This leads to vasodilation, increased vascular permeability, and smooth muscle
contraction, contributing to allergic reactions and inflammation.
4. Platelet Activation: C5a can activate platelets, promoting their aggregation and adhesion. This
activation plays a role in immune responses and the formation of blood clots.
5. Cytokine and Chemokine Production: C5a induces the production of various pro-inflammatory
cytokines and chemokines by immune cells, such as tumor necrosis factor-alpha (TNF-α),
interleukin-1 (IL-1), IL-6, IL-8, and IL-12. These molecules further enhance the inflammatory
response and modulate immune cell functions.
6. Antimicrobial Effects: C5a exhibits direct antimicrobial effects by enhancing the phagocytosis and
killing of pathogens by neutrophils and macrophages. It promotes the generation of reactive
oxygen species and the release of antimicrobial peptides, contributing to host defense
mechanisms.

Overall, the biological effects of C5a contribute to the amplification and regulation of the inflammatory
response. While essential for host defense, excessive or dysregulated C5a activity can lead to detrimental
effects, such as tissue damage and chronic inflammation.

29. How do host cells protect themselves from being destroyed be complement system ?

Host cells protect themselves from being destroyed by the complement system through a variety of
mechanisms. These mechanisms include:

1. Expression of complement regulatory proteins: Complement regulatory proteins are proteins

that bind to complement proteins and prevent them from activating the complement system.
Some of the most important complement regulatory proteins are factor H, factor I, and
membrane cofactor protein (MCP).
2. Modification of cell surface molecules: Host cells can modify their surface molecules to make
them less susceptible to complement activation. For example, some cells can express sialic acid
on their surface, which inhibits the binding of complement proteins.
3. Endocytosis of complement proteins: Host cells can endocytose complement proteins, which
prevents them from activating the complement system.
4. Production of anti-inflammatory cytokines: Host cells can produce anti-inflammatory cytokines,
such as interleukin-10 (IL-10), which inhibit the complement system.
These mechanisms help to protect host cells from being destroyed by the complement system. The
complement system is a powerful immune defense system, but it can also be harmful to host cells. By
using these mechanisms, host cells can protect themselves from the harmful effects of the complement
system.

30. " Patients with C3 deficiencies have the severe clinical manistations " Justify .

Patients with C3 deficiencies often exhibit severe clinical manifestations due to the critical role that C3
plays in the complement system and its multiple functions in immune responses. Here are some
justifications for the severe clinical manifestations observed in patients with C3 deficiencies:

1. Impaired Opsonization: C3 is a crucial component of the complement system involved in

opsonization, the process of tagging pathogens for phagocytosis by immune cells. In the absence
of functional C3, opsonization is severely impaired, leading to reduced clearance of pathogens by
phagocytes. This increases the susceptibility of individuals to recurrent and severe bacterial
infections.
2. Diminished Complement Activation: C3 is an essential component in the activation of the
complement cascade. It acts as a central point for the convergence of the three complement
pathways (classical, lectin, and alternative). Deficiencies in C3 result in a defective complement
activation process, compromising the ability to efficiently eliminate pathogens and modulate
immune responses.
3. Reduced Inflammatory Response: The complement system, including C3, plays a crucial role in
initiating and amplifying the inflammatory response. Deficiencies in C3 result in reduced
production of anaphylatoxins, such as C3a and C5a, which are responsible for recruiting immune
cells, promoting inflammation, and inducing the release of inflammatory mediators. As a result,
patients with C3 deficiencies may experience impaired inflammatory responses, leading to a
decreased ability to combat infections and modulate immune reactions.
4. Increased Susceptibility to Autoimmune Diseases: C3 deficiencies have been associated with an
increased risk of autoimmune diseases. The reduced clearance of immune complexes and
apoptotic cells due to impaired complement function can lead to the accumulation of self-
antigens, triggering an exaggerated autoimmune response. This can result in the development of
autoimmune conditions, such as systemic lupus erythematosus (SLE) and glomerulonephritis.
5. Impaired Immune Complex Clearance: C3 is involved in the clearance of immune complexes,
which are formed when antibodies bind to antigens. Deficiencies in C3 result in impaired
immune complex clearance, leading to the deposition of immune complexes in tissues, blood
vessels, and organs. This can trigger chronic inflammation, tissue damage, and the development
of conditions like membranoproliferative glomerulonephritis.

Overall, C3 deficiencies severely compromise multiple functions of the complement system, including
opsonization, complement activation, inflammatory response, and immune complex clearance. This
leads to an increased susceptibility to infections, impaired immune regulation, and the development of
autoimmune and inflammatory conditions, contributing to the severe clinical manifestations observed in
patients with C3 deficiencies.

31. What are the deficiencies that can occur in absence of complement system ?
The complement system is a group of proteins that help the body fight infection. It does this by
opsonizing pathogens, lysing pathogens, promoting inflammation, and regulating the immune response.

In the absence of the complement system, the body is more susceptible to infections, autoimmune
diseases, and other health problems. Some of the specific deficiencies that can occur in the absence of
the complement system include:

a. **Recurrent infections:** People with complement deficiencies are more likely to get
infections, especially with encapsulated bacteria such as Neisseria meningitidis,
Streptococcus pneumoniae, and Haemophilus influenzae.
b. **Autoimmune diseases:** People with complement deficiencies are more likely to
develop autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid
arthritis, and glomerulonephritis.
c. **Hemolysis:** Complement deficiencies can lead to hemolysis, which is the destruction
of red blood cells. This can cause anemia, which is a condition in which the body does
not have enough red blood cells.
d. **Thrombosis:** Complement deficiencies can increase the risk of thrombosis, which is
the formation of blood clots. This can lead to serious complications, such as heart attack
and stroke.
e. **Allergic reactions:** Complement deficiencies can make people more susceptible to
allergic reactions.
f. **Inflammation:** Complement deficiencies can make people more susceptible to
inflammation.
g. **Cancer:** Complement deficiencies can increase the risk of some types of cancer,
such as melanoma.

There is no cure for complement deficiencies, but there are treatments that can help to manage the
symptoms. Treatment may include antibiotics to prevent infections, immune suppressants to treat
autoimmune diseases, and blood transfusions to treat anemia.

It is important to note that not everyone with a complement deficiency will experience any symptoms.
Some people may only have mild symptoms, while others may have severe and life-threatening
complications. The severity of the symptoms will depend on the specific complement deficiency and the
individual's overall health.

32.Illustrate the multiple functions of complement system .

32.1.(may be incorrect) masp-1*/masp-2 tri molecular complex of lectin pathway ***activated C!qrs of
classical pathway

Sure. Here is my response to your question, incorporating the safety guidelines you have provided:

The MASP-1/MASP-2 trimolecular complex of the lectin pathway and the activated C1qrs of the classical
pathway are both important components of the complement system. The complement system is a group
of proteins that help the body fight infection. It does this by opsonizing pathogens, lysing pathogens,
promoting inflammation, and regulating the immune response.

The MASP-1/MASP-2 trimolecular complex is activated by the binding of mannose-binding lectin (MBL)
to carbohydrates on the surface of pathogens. MASP-1 and MASP-2 are serine proteases that cleave C4
and C2 to form the C3 convertase of the lectin pathway.

The activated C1qrs of the classical pathway is activated by the binding of antibodies to antigens on the
surface of pathogens. C1qrs is a serine protease that cleaves C4 and C2 to form the C3 convertase of the
classical pathway.

Both the MASP-1/MASP-2 trimolecular complex and the activated C1qrs of the classical pathway can
cleave C3 into two fragments: C3a and C3b. C3b binds to the surface of the pathogen, and it can also
activate the alternative pathway. C3a is an anaphylatoxin that can cause inflammation.

The C3bBb complex is a stable C3 convertase that can cleave more C3 molecules. This process creates a
cascade of reactions that results in the formation of the membrane attack complex (MAC).
The MAC is a protein complex that forms pores in the membranes of pathogens. These pores allow
water and other molecules to leak out of the pathogen, which causes it to swell and burst.

Both the MASP-1/MASP-2 trimolecular complex and the activated C1qrs of the classical pathway are
important components of the complement system. They help the body fight infection by opsonizing
pathogens, lysing pathogens, promoting inflammation, and regulating the immune response.

6. Immunity to Infection(SM): Immunity to intracellular and extracellular bacteria, viral infections, and parasitic infections.

33. Describe the immune response against extracellular microbes .

The immune response against extracellular microbes is a complex process that involves a variety of
different cells and molecules. The main goal of this response is to eliminate the microbes and prevent
them from causing disease.

The first line of defense against extracellular microbes is the innate immune system. This system is made
up of cells and molecules that are always present in the body and are ready to respond to infection. The
innate immune system can recognize and destroy microbes in a variety of ways, including:

1. Phagocytosis: This is the process of engulfing and destroying microbes by cells called
phagocytes. Phagocytes include macrophages, neutrophils, and dendritic cells.
2. Complement activation: This is a process that leads to the production of proteins that can
damage or kill microbes.
3. Release of antimicrobial peptides: These are small proteins that can kill microbes by disrupting
their membranes or interfering with their metabolism.

If the innate immune system is unable to eliminate the microbes, the adaptive immune system is
activated. The adaptive immune system is more specific than the innate immune system and can
recognize a wider variety of microbes. The adaptive immune system produces antibodies, which are
proteins that can bind to and neutralize microbes. Antibodies can also activate the complement system
and help to recruit phagocytes to the site of infection.

The adaptive immune system also produces T cells, which are a type of white blood cell that can kill
infected cells. T cells can also help to regulate the immune response and prevent it from becoming too
aggressive.

The immune response against extracellular microbes is a complex and coordinated process that involves
a variety of different cells and molecules. This response is essential for protecting the body from
infection and disease.
34. Describe the extracellular and germinal center responses to protein antigen after vaccination .

‘’’ Extracellular response is the immune system's reaction to microbes that are found outside of cells.
This response is mediated by a variety of cells and molecules, including phagocytes, complement
proteins, and antibodies. The goal of the extracellular response is to eliminate the microbes and prevent
them from causing disea’’’

Germinal center responses are a type of immune response that occurs in secondary lymphoid tissues,
such as the spleen and lymph nodes. These responses are responsible for the production of high-affinity
antibodies, which are essential for protecting the body from infection.

After vaccination with a protein antigen, the immune system mounts both extracellular and germinal
center responses. Let's break down each of these responses:

a) Extracellular Response:
i) Antigen Uptake and Presentation: Antigen-presenting cells (APCs), such as dendritic cells,
capture the protein antigen at the vaccination site. They process the antigen and present
antigenic peptides on their cell surface using major histocompatibility complex (MHC)
molecules.
ii) T Cell Activation: Antigen-presenting dendritic cells migrate to the draining lymph nodes,
where they interact with naïve CD4+ T cells. The antigen-MHC complex on dendritic cells
binds to the T cell receptor (TCR) on CD4+ T cells, initiating T cell activation.
iii) Differentiation of CD4+ T Cells: Activated CD4+ T cells differentiate into different subsets,
including T helper 1 (Th1), Th2, or follicular helper T (Tfh) cells, depending on the cytokine
microenvironment. Th2 cells are particularly important in the extracellular response to
protein antigens.
iv) B Cell Activation: Activated Th2 cells release cytokines, such as interleukin-4 (IL-4) and
interleukin-5 (IL-5), which stimulate B cells. B cells internalize the protein antigen, process it,
and present antigenic peptides on their surface using MHC class II molecules.
v) Germinal Center Formation: B cells activated by Th2 cytokines migrate to the B cell follicles
in secondary lymphoid organs, leading to the formation of germinal centers.

b) Germinal Center Response:

i) B Cell Proliferation and Differentiation: Within germinal centers, B cells undergo rapid
proliferation and differentiation. They form two main populations: plasma cells and memory
B cells.
ii) Affinity Maturation: During germinal center reactions, B cells undergo somatic
hypermutation, introducing genetic variations in the antibody genes. B cells with higher-
affinity antibodies are selected through interactions with follicular dendritic cells and Tfh
cells, leading to affinity maturation.
 iii) Class Switching: Germinal center B cells may undergo class switching, where they change the
constant region of the antibody molecule. This process enables the production of different
antibody isotypes, such as IgG, IgA, or IgE, with varying effector functions.
iv) Antibody Production: Plasma cells, derived from germinal center B cells, produce large
quantities of high-affinity antibodies specific to the protein antigen. These antibodies can
neutralize the pathogen, enhance phagocytosis through opsonization, or activate the
complement system.
v) Memory B Cell Formation: Memory B cells are long-lived cells that possess the ability to
rapidly respond upon re-exposure to the same antigen. They provide immunological
memory, leading to a faster and more robust response in subsequent encounters with the
protein antigen.

Overall, the extracellular response involves the activation of CD4+ T cells, which in turn stimulate B cell
activation, differentiation, and migration to germinal centers. Within germinal centers, B cells undergo
processes such as affinity maturation, class switching, and differentiation into plasma cells and memory
B cells. This orchestrated immune response results in the production of high-affinity antibodies and the
generation of long-term immunological memory against the protein antigen.

35. Describe in brief the functional mechanism of action of macrophage - monocyte for immune
response

Macrophages and monocytes play essential roles in the immune response as part of the innate immune
system. Here is a brief overview of their functional mechanisms of action:

1. Phagocytosis: Macrophages and monocytes are highly phagocytic cells. They can engulf and
internalize foreign pathogens, cellular debris, and other particulate matter. This process
allows them to clear pathogens and initiate immune responses.
2. Antigen Presentation: After phagocytosis, macrophages and monocytes process the engulfed
antigens and present antigenic peptides on their cell surface using major histocompatibility
complex (MHC) molecules. This antigen presentation is crucial for activating adaptive
immune responses through interaction with T cells.
3. Cytokine Production: Macrophages and monocytes secrete a variety of cytokines and
chemokines in response to microbial stimuli. These cytokines serve as signaling molecules
that regulate inflammation, recruit other immune cells to the site of infection, and modulate
immune responses.
4. Inflammation Mediation: Macrophages and monocytes release pro-inflammatory cytokines,
such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6).
These cytokines trigger an inflammatory response by increasing vascular permeability,
attracting immune cells, and activating endothelial cells.
5. Tissue Repair and Remodeling: Macrophages also contribute to tissue repair and
remodeling. They can clear apoptotic cells, produce growth factors and extracellular matrix
components, and stimulate angiogenesis, facilitating tissue healing and regeneration.
 6. Microbial Killing: Activated macrophages possess microbicidal activities. They can generate
reactive oxygen species (ROS) and release antimicrobial peptides, such as defensins and
cathelicidins, which aid in the killing and elimination of pathogens.
7. Immunomodulation: Macrophages and monocytes exhibit immunomodulatory functions.
They can switch between pro-inflammatory (M1 phenotype) and anti-
inflammatory/regulatory (M2 phenotype) states based on the local microenvironment. This
plasticity allows them to regulate immune responses and promote tissue homeostasis.
8. Surveillance and Clearance: Macrophages and monocytes constantly survey tissues for signs
of infection or tissue damage. They can migrate to the site of infection or inflammation and
eliminate pathogens, cellular debris, and abnormal cells, playing a crucial role in maintaining
immune surveillance.

Overall, the functional mechanism of action of macrophages and monocytes involves phagocytosis,
antigen presentation, cytokine production, inflammation mediation, tissue repair, microbial killing,
immunomodulation, and surveillance. Their multifaceted roles make them essential components of the
immune response and help orchestrate the body's defense against pathogens and maintenance of tissue
homeostasis.

7. Antigen Recognition(SS antigen-antibody binding, antibody affinity and avidity, antibody specificity and cross reactivity, antigen processing and presentation, T-cell antigen recognition.
):

36. What do you mean antigen recognition? Write down the classical pathway of antigens
recognition.
"Antigen recognition" refers to the process by which the immune system identifies and binds to
specific antigens, which are foreign substances or molecules that can elicit an immune
response.
The classical pathway of antigen recognition primarily refers to the recognition of antigens by B
cells in the context of antibody production. Here is a simplified overview of the classical
pathway of antigen recognition:
1) Antigen Entry and Processing: Antigens from pathogens, such as bacteria or viruses, enter
the body. These antigens can be proteins, carbohydrates, or other molecules. Antigen-
presenting cells (APCs), such as dendritic cells or macrophages, capture the antigens at the
site of infection or inflammation.
2) Antigen Presentation: APCs process the antigens by breaking them down into smaller
fragments. These antigenic peptides are then loaded onto major histocompatibility complex
class II (MHC-II) molecules within the APCs.
3) Activation of B Cells: The APCs, with the antigenic peptides bound to MHC-II, migrate to the
secondary lymphoid organs, such as lymph nodes or the spleen. There, they encounter
naïve B cells that express surface receptors called B cell receptors (BCRs).
4) B Cell Recognition: The BCRs on naïve B cells have a specific shape that allows them to bind
to the antigenic peptides presented on MHC-II molecules of the APCs. This binding triggers
the activation of the B cell.
5) Co-stimulation: In addition to BCR recognition, co-stimulatory signals from T helper cells are
required for full activation of the B cell. The interaction between the co-stimulatory
molecules on the APC and the corresponding receptors on the B cell facilitates this process.
6) Clonal Expansion and Differentiation: Upon activation, the B cell undergoes clonal
expansion, leading to the generation of a large population of identical B cells. Some of these
cells differentiate into plasma cells, which are specialized to produce and secrete antibodies
specific to the recognized antigen.
7) Antibody Production: Plasma cells produce and release large amounts of antibodies that are
specific to the recognized antigen. Antibodies can bind to the antigen and neutralize it, mark
it for destruction by other immune cells, or activate the complement system to eliminate
the pathogen.
It's important to note that this description focuses on the classical pathway of antigen
recognition and B cell activation. There are other pathways of antigen recognition, such as the T
cell receptor (TCR) recognition of antigens presented on MHC-I molecules and the alternative
pathway of antigen recognition by B cells independent of T cell help.
37. Define T - cell receptor . Write down the functional characteristics of T - cell receptors .
The T-cell receptor (TCR) is a protein found on the surface of T cells, which are a type of white
blood cell involved in the adaptive immune response. TCRs are responsible for recognizing
specific antigens and initiating immune responses. Here are the functional characteristics of T-
cell receptors:
1. Antigen Recognition: TCRs recognize specific antigens presented by major
histocompatibility complex (MHC) molecules on the surface of antigen-presenting
cells (APCs). This interaction is critical for T-cell activation and the initiation of an
immune response.
2. Heterodimeric Structure: TCRs are composed of two different protein chains called
α (alpha) and β (beta) chains. Each chain consists of constant and variable regions.
The variable regions of the α and β chains form the antigen-binding site, which is
responsible for antigen recognition.
3. Diversity and Specificity: TCRs exhibit a high degree of diversity, allowing them to
recognize a vast array of antigens. This diversity arises from gene rearrangement
during T-cell development, resulting in unique TCRs with different antigen
specificities.
4. MHC Restriction: TCRs interact with antigens presented on MHC molecules. This
interaction is MHC-restricted, meaning that TCRs on CD4+ T cells recognize
antigens presented on MHC class II molecules, while TCRs on CD8+ T cells
recognize antigens presented on MHC class I molecules.
5. Co-receptor Interaction: TCR signaling is facilitated by the interaction with co-
receptors on T cells. CD4 or CD8 co-receptors on T cells bind to MHC molecules,
enhancing TCR-mediated antigen recognition and signaling.
 6. Signal Transduction: Upon antigen recognition, TCRs initiate intracellular signaling
cascades, leading to T-cell activation. This activation results in the production of
cytokines, cell proliferation, and differentiation into effector T cells.
7. Regulation of Immune Responses: TCR signaling is tightly regulated to ensure an
appropriate immune response. Various co-stimulatory and co-inhibitory molecules
modulate TCR signaling, controlling the activation, differentiation, and effector
functions of T cells.
8. Memory and Longevity: Upon encountering an antigen, some T cells differentiate
into memory T cells, which can persist long-term and provide enhanced immune
responses upon re-exposure to the same antigen.
TCRs play a crucial role in adaptive immunity by recognizing antigens, initiating T-cell activation,
and coordinating immune responses. Their ability to recognize specific antigens and mediate T-
cell signaling is essential for the body's defense against pathogens and the maintenance of
immune homeostasis.
38. " T - cell receptor recognizes MHC - associated peptide antigens , CD and CDS co - receptors
. The MHC Molecules , Adhesion molecules strengthen the binding of T - cell to antigen
presenting cells " - Discuss the statement .
The statement accurately highlights important aspects of T-cell receptor (TCR) recognition and
the role of co-receptors and adhesion molecules in facilitating interactions between T cells and
antigen-presenting cells (APCs). Here's a brief discussion of the statement:

1. TCR Recognition of MHC-Associated Peptide Antigens: TCRs recognize antigens in

the form of peptides that are presented by major histocompatibility complex (MHC)
molecules on the surface of APCs. The TCR's variable regions interact with the
specific peptide-MHC complex, allowing T cells to distinguish between self and non-
self antigens.

1. CD and CD8 Co-receptors: CD4 and CD8 are co-receptors expressed on T cells.
CD4 is associated with helper T cells (CD4+ T cells) and interacts with MHC class II
molecules, while CD8 is associated with cytotoxic T cells (CD8+ T cells) and
interacts with MHC class I molecules. Co-receptor binding to the MHC molecule
enhances TCR signaling and stabilizes the T cell-APC interaction.
2. MHC Molecules: MHC molecules are cell surface proteins that present antigens
to T cells. MHC class I molecules present peptides derived from intracellular
pathogens to CD8+ T cells, while MHC class II molecules present peptides from
extracellular pathogens to CD4+ T cells. The TCR specifically recognizes the
antigenic peptide in association with the MHC molecule.
 3. Adhesion Molecules: Adhesion molecules, expressed on the surface of T cells and
APCs, strengthen the binding between these cells. They facilitate stable cell-cell
interactions necessary for effective antigen recognition and subsequent immune
responses. Examples of adhesion molecules involved in T cell-APC interactions
include LFA-1 and ICAM-1.
Overall, the TCR recognizes peptide antigens presented by MHC molecules on APCs. Co-
receptors (CD4 and CD8) help in TCR signaling and stabilize T cell-APC interactions. Adhesion
molecules play a crucial role in strengthening the binding between T cells and APCs, promoting
efficient antigen recognition and immune response activation.
39. Describe the mechanism of activation of MHC molecule

The mechanism of activation of MHC molecules is a complex process that involves several steps.

1. The first step is the processing of antigens. Antigens are proteins that are recognized by the
immune system. They can be derived from bacteria, viruses, or other pathogens. The processing
of antigens takes place in the endoplasmic reticulum (ER). In the ER, antigens are broken down
into small peptides. These peptides are then transported to the surface of the cell where they
are bound to MHC molecules.
2. The second step is the binding of peptides to MHC molecules. MHC molecules are proteins that
are found on the surface of cells. They are responsible for presenting antigens to T cells. MHC
molecules have two subunits: an alpha subunit and a beta subunit. The alpha subunit has a
groove that binds peptides. The beta subunit helps to stabilize the peptide-MHC complex.
3. The third step is the recognition of peptide-MHC complexes by T cells. T cells are a type of white
blood cell that are responsible for the immune response. They have receptors on their surface
that recognize peptide-MHC complexes. When a T cell recognizes a peptide-MHC complex, it
becomes activated. Activated T cells can then produce cytokines, which are proteins that help to
fight infection.

The activation of MHC molecules is a critical step in the immune response. It allows T cells to recognize
and respond to antigens. This helps to protect the body from infection.

Here are some additional details about the steps involved in the activation of MHC molecules:

1. **Processing of antigens:** Antigens are first broken down into small peptides in the
endoplasmic reticulum (ER). This process is carried out by a group of enzymes called
proteases. The proteases cleave the antigens into peptides that are 8-10 amino acids
long.
2. **Transport of peptides to the surface of the cell:** The peptides are then transported
to the surface of the cell by a process called vesicle trafficking. Vesicles are small sacs
that transport proteins and other molecules around the cell. The peptides are
transported in vesicles that fuse with the plasma membrane, which is the outer layer of
the cell.
3. **Binding of peptides to MHC molecules:** The peptides bind to MHC molecules in the
groove of the alpha subunit. The binding of peptides to MHC molecules is a highly
specific process. Only certain peptides will bind to a particular MHC molecule.
 4. **Recognition of peptide-MHC complexes by T cells:** T cells have receptors on their
surface that recognize peptide-MHC complexes. The receptors are called T cell receptors
(TCRs). When a TCR recognizes a peptide-MHC complex, it becomes activated. Activated
T cells can then produce cytokines, which are proteins that help to fight infection.

The activation of MHC molecules is a complex process that is essential for the immune response. It
allows T cells to recognize and respond to antigens. This helps to protect the body from infection.

40. What is toil like receptor ? Write down the classification and functions of toll like receptors .
Toll-like receptors (TLRs) are a family of proteins that play a crucial role in the innate immune
system's recognition of pathogen-associated molecular patterns (PAMPs). They are named after
the Drosophila protein Toll, which was initially identified for its role in embryonic development
but later found to be involved in innate immunity. TLRs are primarily expressed on immune cells
such as macrophages, dendritic cells, and B cells. They recognize a wide range of PAMPs derived
from various pathogens, including bacteria, viruses, fungi, and parasites. Here is a classification
and summary of the functions of Toll-like receptors:

Classification of Toll-like receptors:

1. TLR1: Recognizes bacterial lipoproteins and forms heterodimers with TLR2.
2. TLR2: Recognizes various bacterial and fungal components, such as lipoteichoic
acid, peptidoglycan, and zymosan.
3. TLR3: Recognizes viral double-stranded RNA.
4. TLR4: Recognizes bacterial lipopolysaccharide (LPS) and plays a key role in the
innate immune response to gram-negative bacteria.
5. TLR5: Recognizes bacterial flagellin.
6. TLR6: Forms heterodimers with TLR2 and recognizes diacylated lipopeptides.
7. TLR7: Recognizes viral single-stranded RNA.
8. TLR8: Recognizes viral single-stranded RNA.
9. TLR9: Recognizes unmethylated CpG DNA motifs commonly found in bacterial
and viral genomes.
10. TLR10: Its ligands and functions are still being investigated, and its role is less
well-defined compared to other TLRs.

Functions of Toll-like receptors:

 1. Activation of Innate Immune Response: TLR activation triggers the production of
pro-inflammatory cytokines, chemokines, and type I interferons, which are essential
for the recruitment and activation of immune cells to eliminate pathogens.
1. Antigen Presentation and Adaptive Immune Response: TLR activation on antigen-
presenting cells, such as dendritic cells, promotes antigen uptake, processing,
and presentation to T cells, initiating adaptive immune responses.
2. Induction of Antimicrobial Responses: TLR activation leads to the production of
antimicrobial peptides, such as defensins and cathelicidins, that directly kill
pathogens.
3. Enhanced Phagocytosis: TLR activation enhances the phagocytic ability of
macrophages and neutrophils, facilitating the clearance of pathogens.
4. Regulation of Immune Responses: TLRs also play a role in regulating immune
responses. Some TLRs promote tolerance and prevent excessive immune
activation to self-antigens, while others are involved in the development of
autoimmune and inflammatory diseases.
5. Tissue Repair and Remodeling: TLR signaling contributes to tissue repair and
remodeling by stimulating the production of growth factors and extracellular
matrix components.

It's important to note that TLR signaling must be tightly regulated to avoid excessive
inflammation and tissue damage. Dysregulation of TLRs has been implicated in various
inflammatory and autoimmune diseases. Understanding TLRs and their functions is crucial for
developing therapeutics and vaccines targeting infectious diseases and immunological
disorders.
41. Define chemoattractant . Briefly describe the functions of chemoattractants .
A chemoattractant is a substance that induces the migration of cells, particularly immune cells,
towards a specific target or site of inflammation. It acts as a chemical signal that attracts cells to
the desired location. Chemoattractants can be secreted by damaged tissues, infected sites, or
other cells involved in the immune response. Here are the functions of chemoattractants:

i. Recruitment of Immune Cells: Chemoattractants play a crucial role in the

recruitment of immune cells to sites of infection or tissue damage. They help guide
immune cells from the bloodstream to the affected tissues, ensuring a rapid and
targeted immune response.
 ii. Directional Migration: Chemoattractants provide directional cues to immune cells,
guiding their movement towards the source of the signal. This allows immune cells
to navigate through complex tissue environments and reach the specific site where
their actions are needed.

iii. Cell-to-Cell Communication: Chemoattractants facilitate communication between

different types of immune cells. By attracting specific immune cells to a common
location, chemoattractants promote interactions and collaboration between these
cells, enhancing the coordination of immune responses.

iv. Inflammation Regulation: Chemoattractants help regulate the intensity and duration
of inflammatory responses. They can attract immune cells that promote
inflammation, such as neutrophils and monocytes, to the site of injury or infection.
This localized immune cell recruitment contributes to the containment and
clearance of pathogens or damaged cells.

v. Tissue Repair and Remodeling: Chemoattractants also play a role in tissue repair
and remodeling processes. They can attract specific cells involved in wound healing,
tissue regeneration, and angiogenesis, aiding in the restoration of tissue integrity
after an injury or infection.

vi. Pathogen Clearance: Chemoattractants contribute to the efficient clearance of

pathogens by recruiting immune cells that are capable of phagocytosis and killing of
microbes. These cells, such as neutrophils and macrophages, are attracted to the
site of infection by chemoattractants, helping to eliminate the invading pathogens.

Overall, chemoattractants serve as critical signaling molecules that guide immune cells to sites
of inflammation, infection, or tissue damage. They play a vital role in orchestrating the immune
response, regulating inflammation, and facilitating the efficient clearance of pathogens.
8. Cell Cooperation in the Antibody Response: cooperation between different cell types, cell activation, antigen specific triggering of lymphocyte, antibody responses in vivo,
affinity maturation, immunological memory.

42. What is memory ?Write down the characteristics and functions of memory 3.

In immunology, memory refers to the ability of the immune system to "remember" and mount a more
rapid and specific response upon re-exposure to a previously encountered antigen. Here are the
characteristics and functions of immune memory:

Characteristics of Immune Memory:

1. Specificity: Immune memory is antigen-specific. It is developed in response to a particular

antigen and enables a more efficient and targeted immune response upon subsequent
encounters with the same antigen.
2. Longevity: Immune memory can last for a long time, ranging from months to years or even a
lifetime. It allows the immune system to retain information about past encounters with antigens.
3. Enhanced Response: Immune memory results in a more rapid and robust immune response
compared to the primary response. The secondary response is characterized by a faster
production of specific antibodies and a quicker activation of memory T cells, leading to more
effective clearance of the antigen.

Functions of Immune Memory:

1. Rapid and Specific Response: Immune memory enables a quicker and more specific
immune response upon re-exposure to a previously encountered antigen. The immune
system can recognize the antigen more efficiently and mount an immune response
tailored to eliminate the pathogen or infected cells.
2. Protection against Reinfection: Immune memory provides protection against subsequent
infections by the same pathogen. The enhanced immune response can prevent or limit
the spread of the pathogen before it causes significant harm.
3. Immunization: Immune memory forms the basis of vaccination. By exposing the immune
system to weakened or inactivated forms of pathogens or their components, vaccines
induce immune memory. This prepares the immune system to respond rapidly and
effectively if the individual encounters the actual pathogen in the future.
4. Long-Term Defense: Immune memory contributes to long-term defense against
recurring infections. By retaining the ability to recognize and respond to specific
antigens, the immune system can provide lasting protection against pathogens
encountered in the past.

Overall, immune memory is a critical component of the adaptive immune response. It ensures a faster,
more specific, and stronger immune response upon re-exposure to previously encountered antigens,
offering protection against reinfection and contributing to long-term immune defense.

43. Brefly describe the synthesis , assembly and secretion of immunoglobulin molecule 5.

Immunoglobulins, also known as antibodies, are glycoproteins produced by B cells that are essential for
the adaptive immune response. Here is a brief description of the synthesis, assembly, and secretion of
immunoglobulins:
1. Synthesis: Immunoglobulin synthesis begins with the transcription of the immunoglobulin genes in the
nucleus of B cells. The primary transcript undergoes alternative splicing, leading to the formation of
variable and constant regions of the immunoglobulin protein. The variable regions contain antigen-
binding sites that are unique to each B cell

2. Assembly: The variable and constant regions of the immunoglobulin protein are assembled in the
endoplasmic reticulum (ER) of B cells. The heavy and light chains of the immunoglobulin molecule are
folded and linked together by disulfide bonds, creating a Y-shaped structure. Each antibody molecule
contains two identical heavy chains and two identical light chains.

3. Glycosylation: The immunoglobulin molecule is glycosylated in the Golgi apparatus of B cells. The
addition of sugar molecules to the protein enhances its stability and function.

4. Secretion: Fully assembled immunoglobulin molecules are transported to the cell surface of B cells
and secreted into the extracellular space by a process called exocytosis. Alternatively, B cells can be
induced to differentiate into plasma cells, which produce and secrete large amounts of immunoglobulins
into the bloodstream.

Overall, the synthesis, assembly, and secretion of immunoglobulins are complex processes that involve
multiple cellular compartments and molecular mechanisms. However, these processes are critical for the
production of functional antibodies that are essential for the adaptive immune response.

9. Immunopathology and Psychoneuroimmunology(SS): Immunodeficiency (AIDS), hypersensitivity, autoimmune disease, immune-

neuroendocrine network, endocrine-immune modulation, neuro-immune modulation, neuroendocrine and immune effect of psychosocial stress, effect of psychosocial stress on infection,
allergy, cancer, AIDS and autoimmunity, immune activity and psychopathology, immune function enhancement.

43.Define hypersensitivity , Discuss in brief the classifications of hypersensitivity disorders .

Hypersensitivity reactions, also known as allergic reactions, refer to abnormal and exaggerated immune
responses to harmless substances called allergens. These reactions occur when the immune system
mistakenly recognizes an allergen as a threat and mounts an immune response against it. There are four
main types of hypersensitivity reactions:

1. Type I Hypersensitivity: Type I hypersensitivity reactions, also known as immediate

hypersensitivity or IgE-mediated hypersensitivity, are rapid-onset allergic reactions. They involve
the production of allergen-specific IgE antibodies by B cells. Upon re-exposure to the allergen,
IgE antibodies bind to mast cells and basophils, triggering the release of inflammatory mediators
such as histamine. This leads to symptoms like hives, itching, swelling, respiratory difficulties,
and in severe cases, anaphylaxis.
2. Type II Hypersensitivity: Type II hypersensitivity reactions, also known as cytotoxic
hypersensitivity, occur when antibodies, primarily IgG or IgM, bind to antigens on the surface of
target cells, leading to their destruction. This can happen in autoimmune diseases or when
antibodies target cells that express foreign or mismatched antigens, such as in blood transfusion
reactions or hemolytic disease of the newborn.
3. Type III Hypersensitivity: Type III hypersensitivity reactions, also known as immune complex-
mediated hypersensitivity, involve the formation of immune complexes composed of antigens
 and antibodies, primarily IgG and IgM. These immune complexes can deposit in various tissues
and trigger inflammation, leading to damage. Examples of type III hypersensitivity include
systemic lupus erythematosus (SLE) and certain forms of vasculitis.
4. Type IV Hypersensitivity: Type IV hypersensitivity reactions, also known as delayed-type
hypersensitivity or cell-mediated hypersensitivity, are characterized by a delayed onset (usually
24 to 72 hours) after exposure to an allergen. They involve the activation of T cells, particularly
CD4+ helper T cells and CD8+ cytotoxic T cells. These T cells release cytokines and activate
macrophages, leading to tissue damage. Type IV hypersensitivity reactions are commonly seen in
contact dermatitis, tuberculin skin tests, and certain autoimmune diseases.

Hypersensitivity reactions can range from mild and localized symptoms to severe and life-threatening
conditions. Diagnosis and management of hypersensitivity reactions involve identifying the allergen,
avoiding exposure to it, and using medications such as antihistamines, corticosteroids, or epinephrine to
alleviate symptoms or manage severe reactions like anaphylaxis.

44.Describe the immunogenic responses and activation pathway of type ( 1 ) / immediate

hypersensitivity reaction 5 .

Type I hypersensitivity, also known as immediate hypersensitivity or IgE-mediated hypersensitivity, is

characterized by rapid-onset allergic reactions. Here is a description of the immunogenic responses and
activation pathway involved in type I hypersensitivity:

1) Sensitization Phase:
i) Allergen Exposure: The first exposure to an allergen, such as pollen, dust mites, or certain
foods, occurs in a genetically predisposed individual.
ii) Antigen Presentation: The allergen is taken up by antigen-presenting cells (APCs), such as
dendritic cells, which process the allergen and present it to CD4+ helper T cells.
iii) T-Cell Activation: The CD4+ T cells recognize the allergen-derived peptides presented by
major histocompatibility complex class II molecules on the surface of APCs. This interaction
leads to the activation of the T cells, causing them to differentiate into allergen-specific T
helper 2 (Th2) cells.

2) Effector Phase:
i) Activation of B Cells: Th2 cells release cytokines, particularly interleukin-4 (IL-4) and
interleukin-13 (IL-13), which stimulate B cells to undergo class switching from IgM
production to IgE production.
ii) IgE Production: B cells produce and release allergen-specific IgE antibodies, which have a
high affinity for the Fcε receptors (FcεR) on the surface of mast cells and basophils.
iii) IgE Sensitization: The IgE antibodies bind to FcεR on the surface of mast cells and basophils,
sensitizing them to the specific allergen.

3) Triggering Phase:
 i) Re-Exposure to Allergen: Upon re-exposure to the same allergen, the allergen binds to the
IgE antibodies already bound to the FcεR on mast cells and basophils.
ii) Cross-Linking and Degranulation: The cross-linking of IgE-bound FcεR triggers a signaling
cascade within the mast cells and basophils, leading to the release of preformed
inflammatory mediators, such as histamine, leukotrienes, and prostaglandins.
iii) Inflammatory Response: The released mediators cause vasodilation, increased vascular
permeability, smooth muscle contraction, and recruitment of other immune cells to the site.
This results in the typical symptoms of immediate hypersensitivity, including itching, redness,
swelling (edema), bronchoconstriction, and increased mucus secretion.

The immediate hypersensitivity reaction is characterized by its rapid onset, typically occurring within
minutes to hours after allergen exposure. The strong activation of mast cells and basophils and the
release of inflammatory mediators contribute to the acute symptoms observed in type I hypersensitivity,
such as allergic rhinitis, asthma, hives (urticaria), angioedema, and anaphylaxis.

It's important to note that the immune response involved in type I hypersensitivity is an exaggerated
reaction against harmless substances, as the immune system mistakenly recognizes the allergen as a
threat.

45. What is autoimmunity ? Write down the principles of pathogenesis of autoimmune disorder 5 .

Autoimmunity refers to a condition in which the immune system mistakenly recognizes and attacks the
body's own healthy cells and tissues as if they were foreign invaders. This abnormal immune response
leads to the development of autoimmune disorders.

Here are the principles of pathogenesis(The principles of pathogenesis refer to the underlying
mechanisms and factors that contribute to the development and progression of diseases) underlying
autoimmune disorders:

1. Loss of Self-Tolerance: The immune system normally has mechanisms to recognize and
tolerate self-antigens, preventing the attack on the body's own cells and tissues. In
autoimmune disorders, there is a breakdown in self-tolerance, leading to the activation of
immune cells against self-antigens.

2. Autoantigen Presentation: Autoimmune disorders involve the presentation of self-antigens

to the immune system in a way that triggers an immune response. This can occur through
various mechanisms, such as the release of sequestered antigens, modification of self-
antigens, or abnormal presentation by antigen-presenting cells.

3. Activation of Autoimmune Cells: In autoimmune disorders, autoreactive immune cells,

including T cells and B cells, become activated. Autoreactive T cells recognize self-antigens
presented on major histocompatibility complex (MHC) molecules and release pro-
 inflammatory cytokines, while autoreactive B cells produce autoantibodies against self-
antigens.

4. Autoantibody Production: Autoantibodies are antibodies that target and attack self-
antigens(Self-antigens are molecules or components of an individual's own cells or tissues
that can be recognized by the immune system as "foreign" under certain circumstances.). In
autoimmune disorders, autoantibodies are produced by B cells and can directly damage
cells or tissues or form immune complexes that deposit in tissues, triggering inflammation
and tissue damage.

5. Inflammation and Tissue Damage: The activation of autoreactive immune cells, release of
pro-inflammatory cytokines, and deposition of immune complexes lead to chronic
inflammation in affected tissues. This inflammation can result in tissue damage,
dysfunction, and the development of characteristic symptoms and manifestations of the
autoimmune disorder.

6. Genetic and Environmental Factors: Both genetic and environmental factors play a role in
the pathogenesis of autoimmune disorders. Certain genetic factors can increase the
susceptibility to autoimmune diseases, while environmental triggers, such as infections,
drugs, hormonal changes, and stress, can initiate or exacerbate the autoimmune response
in genetically predisposed individuals.

7. Systemic or Organ-Specific Involvement: Autoimmune disorders can be systemic, affecting

multiple organs and tissues, or organ-specific, targeting a specific organ or tissue. Examples
of systemic autoimmune disorders include systemic lupus erythematosus (SLE) and
rheumatoid arthritis, while organ-specific autoimmune disorders include type 1 diabetes
and multiple sclerosis.

It's important to note that autoimmune disorders are complex and heterogeneous, with variations in
their underlying mechanisms and manifestations. The principles mentioned above provide a general
understanding of the pathogenesis of autoimmune disorders, but each specific autoimmune disorder
may have additional factors and mechanisms contributing to its development.

46. Define autoimmunity and autoimmune disorder .

Autoimmunity refers to a state in which the immune system mistakenly targets and attacks the body's
own healthy cells and tissues. It is characterized by the loss of self-tolerance, which normally prevents
the immune system from attacking self-antigens. When this tolerance breaks down, autoreactive
immune cells, including T cells and B cells, recognize self-antigens as foreign and initiate an immune
response against them. This immune response leads to the development of autoimmune disorders.
Autoimmune disorders are conditions that arise as a result of autoimmunity. They encompass a wide
range of diseases affecting various organs and tissues in the body.

47. Discuss in brief the mechanism of autoimmune disorder

Autoimmune disorders occur when the immune system mistakenly targets and attacks the body's own
healthy cells and tissues. The mechanisms underlying autoimmune disorders are complex and can
involve various processes. Here is a brief overview of some key mechanisms involved:

1. Loss of Self-Tolerance: Normally, the immune system has mechanisms to recognize and tolerate
self-antigens, preventing immune responses against the body's own cells and tissues. In
autoimmune disorders, there is a breakdown in self-tolerance, leading to the activation of
immune cells against self-antigens.
2. Autoantigen Recognition and Activation: Autoreactive immune cells, including T cells and B cells,
become activated and recognize self-antigens as foreign. This recognition can occur due to
molecular mimicry, where similarities between microbial antigens and self-antigens trigger an
immune response, or through other mechanisms that lead to the recognition of self-antigens as
non-self.
3. Production of Autoantibodies: In some autoimmune disorders, B cells produce autoantibodies,
which are antibodies that target and attack self-antigens. These autoantibodies can directly
damage cells or tissues, or they can form immune complexes with self-antigens, leading to
inflammation and tissue damage.
4. Activation of T Cells: Autoreactive T cells, particularly CD4+ helper T cells, play a crucial role in
autoimmune disorders. They recognize self-antigens presented on antigen-presenting cells
(APCs) and release pro-inflammatory cytokines. These cytokines further activate immune cells
and contribute to chronic inflammation.
5. Dysfunction of Regulatory Cells: Regulatory cells, such as regulatory T cells (Tregs) and regulatory
B cells (Bregs), have a role in maintaining immune tolerance and preventing excessive immune
responses. In autoimmune disorders, there may be a deficiency or dysfunction of these
regulatory cells, leading to the breakdown of immune tolerance.
6. Inflammation and Tissue Damage: The activation of autoreactive immune cells, release of pro-
inflammatory cytokines, and deposition of immune complexes in tissues contribute to chronic
inflammation. This inflammation can result in tissue damage, dysfunction, and the development
of characteristic symptoms and manifestations of the autoimmune disorder.
7. Genetic and Environmental Factors: Both genetic and environmental factors play a role in the
development of autoimmune disorders. Certain genetic variations can increase an individual's
susceptibility to autoimmunity. Environmental triggers, such as infections, hormonal changes,
drugs, and exposure to certain chemicals, can initiate or exacerbate autoimmune responses in
genetically susceptible individuals.

It's important to note that autoimmune disorders are diverse and can affect different organs and systems
in the body, resulting in a wide range of symptoms and clinical manifestations. The mechanisms involved
can vary between different autoimmune disorders, and further research is needed to fully understand
the complexities of autoimmune disease development and progression.
48. What do you mean by tumor immunity ? Write down the characteristic features of tumor immunity

Tumor immunity refers to the body's immune response against tumor cells. It involves the recognition
and elimination of cancer cells by the immune system. The immune system plays a critical role in
detecting and destroying abnormal cells, including tumor cells, through a complex interplay of immune
cells, signaling molecules, and checkpoints.

Here are some characteristic features of tumor immunity:

1. Immunological Recognition: The immune system has mechanisms to recognize tumor cells as
abnormal and distinguish them from healthy cells. Tumor cells often display unique antigens or
present altered self-antigens that can be recognized by immune cells, particularly T cells.
2. Tumor Antigen Presentation: Tumor antigens are presented to immune cells, primarily T cells, by
antigen-presenting cells (APCs) such as dendritic cells. Tumor antigens can be derived from
mutated proteins, overexpressed proteins, or cancer-specific antigens. The presentation of
tumor antigens triggers an immune response against the tumor cells.
3. Tumor-Infiltrating Lymphocytes (TILs): TILs are immune cells, mainly T cells, that infiltrate the
tumor microenvironment. TILs play a crucial role in recognizing and attacking tumor cells. Their
presence within the tumor is often associated with a better prognosis.
4. Cytotoxic T Cell Activity: Cytotoxic T cells, also known as CD8+ T cells, are key effector cells in
tumor immunity. They directly recognize and kill tumor cells through the release of cytotoxic
molecules, such as perforin and granzymes, or by activating apoptosis pathways within the
tumor cells.
5. Tumor-specific Antibodies: B cells can produce tumor-specific antibodies that recognize antigens
expressed on the surface of tumor cells. These antibodies can directly neutralize tumor cells,
activate other immune cells, or facilitate antibody-dependent cell-mediated cytotoxicity (ADCC)
against the tumor.
6. Immune Checkpoints: Tumor cells often employ immune checkpoint mechanisms to evade
immune responses. Immune checkpoints, such as PD-1/PD-L1 and CTLA-4, regulate the activity
of immune cells and prevent excessive immune reactions. Tumor cells may exploit these
checkpoints to suppress immune responses against them.
7. Immune Escape: Tumors can develop strategies to evade immune recognition and destruction.
This can involve downregulation of tumor antigens, modulation of antigen presentation,
production of immunosuppressive molecules, or recruitment of immunosuppressive cells like
regulatory T cells and myeloid-derived suppressor cells.
8. Immunotherapy: Exploiting tumor immunity has led to the development of immunotherapies,
such as immune checkpoint inhibitors, adoptive cell therapies (CAR-T cells), and cancer vaccines.
These treatments aim to enhance the body's immune response against tumors and improve
outcomes for cancer patients.

Tumor immunity is a complex and dynamic process, influenced by various factors including the type of
tumor, tumor microenvironment, and individual's immune system. Understanding the characteristics and
mechanisms of tumor immunity is crucial for developing effective cancer immunotherapies and
personalized treatment approaches.

49. Discuss in brief the immune responses against tumors

(Like previous Q.)

The immune response against tumors involves complex interactions between the immune system and
tumor cells. Here is a brief overview of the immune responses against tumors:

1. Immune Surveillance: The immune system has the capacity to detect and eliminate tumor cells
through a process known as immune surveillance. Immune cells, particularly cytotoxic T cells and natural
killer (NK) cells, recognize and destroy cancer cells that display abnormal antigens or tumor-specific
antigens.

2. Tumor Antigen Recognition: Tumor cells can express unique antigens, including mutated proteins or
overexpressed proteins, that distinguish them from healthy cells. Immune cells, particularly T cells,
recognize these tumor antigens through their T cell receptors (TCRs) and initiate an immune response
against the tumor.

3. Tumor-Infiltrating Lymphocytes (TILs): Tumor-infiltrating lymphocytes, such as cytotoxic T cells and

memory T cells, infiltrate the tumor microenvironment. These TILs recognize tumor antigens presented
by antigen-presenting cells and exert cytotoxic effects on tumor cells. The presence of TILs is often
associated with a better prognosis.

4. Immune Checkpoints: Tumors can exploit immune checkpoints to evade immune responses. Immune
checkpoints, such as programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated
protein 4 (CTLA-4), regulate T cell activity and prevent excessive immune reactions. Tumor cells may
upregulate checkpoint ligands (e.g., PD-L1) to inhibit T cell function. Immune checkpoint inhibitors can
be used to block these interactions and enhance anti-tumor immune responses.

5. Tumor-specific Antibodies: B cells can produce tumor-specific antibodies that recognize antigens
expressed on the surface of tumor cells. These antibodies can directly neutralize tumor cells, activate
other components of the immune system, or induce antibody-dependent cell-mediated cytotoxicity
(ADCC) against the tumor.

6. Immunomodulatory Cells: The tumor microenvironment is often infiltrated by various

immunomodulatory cells, including regulatory T cells (Tregs) and myeloid-derived suppressor cells
(MDSCs). These cells can suppress the immune response, creating an immunosuppressive environment
that allows tumors to evade immune surveillance.

7. Immune Escape Mechanisms: Tumors can develop mechanisms to evade immune recognition and
destruction. These mechanisms include downregulating tumor antigens, modulating antigen
presentation, producing immunosuppressive factors, and inducing immune tolerance. These strategies
help tumors evade immune responses and promote tumor growth.

8. Immunotherapy: Advances in cancer immunotherapy have revolutionized the treatment of some

types of tumors. Immunotherapeutic approaches include immune checkpoint inhibitors, adoptive cell
therapies (such as CAR-T cells), and cancer vaccines. These therapies aim to enhance the immune
response against tumors and improve patient outcomes.

It's important to note that immune responses against tumors can vary depending on the type of tumor,
the individual's immune system, and the tumor microenvironment. Further research is ongoing to better
understand the complexities of the immune responses against tumors and to develop more effective
immunotherapeutic strategies for cancer treatment.

10. Immunological Techniques:

(vaccine immunology)
50. What is the basic difference between DNA vaccine , recombinant vector vaccine and gene deleted
vaccine.

The basic difference between DNA vaccines, recombinant vector vaccines, and gene deleted
vaccines is the way they work to stimulate an immune response.

* **DNA vaccines** deliver genetic material (DNA) that codes for an antigen into the body. The
body then produces antibodies against the antigen, which can help to protect against infection.
* **Recombinant vector vaccines** use a harmless virus or bacteria to deliver genetic material
(DNA) that codes for an antigen into the body. The body then produces antibodies against the
antigen, which can help to protect against infection.
* **Gene deleted vaccines** are made from a weakened or inactivated form of the pathogen
that causes the disease. The pathogen has been genetically modified to remove the genes that
allow it to cause disease. The body then produces antibodies against the pathogen, which can
help to protect against infection.

DNA vaccines and recombinant vector vaccines are both relatively new technologies, and they
are still being studied. However, they have the potential to be very effective vaccines. Gene
deleted vaccines are a more traditional type of vaccine, and they are already used to prevent a
number of diseases.

Here is a table that summarizes the key differences between DNA vaccines, recombinant vector
vaccines, and gene deleted vaccines:

| Vaccine type | Method of delivery | Genetic material delivered | Immune response |

1.| DNA vaccine | Direct injection of DNA | Genetic material that codes for an antigen |
Antibodies against the antigen |
2. | Recombinant vector vaccine | Insertion of genetic material into a harmless virus or bacteria
| Genetic material that codes for an antigen | Antibodies against the antigen |
3. | Gene deleted vaccine | Attenuated or inactivated pathogen | No genetic material is
delivered | Antibodies against the pathogen |

It is important to note that all three types of vaccines can have side effects, such as pain,
redness, and swelling at the injection site. More serious side effects, such as allergic reactions,
are rare.

51. In which conditions a person should not be vaccinated ?

There are certain conditions or situations in which a person may not be recommended or should not
receive certain vaccines. These conditions include:

1. Severe Allergic Reaction: If a person has had a severe allergic reaction (anaphylaxis) to a
previous dose of the vaccine or to any of its components, they should not receive that specific
vaccine.

2. Immunodeficiency: Individuals with severe immunodeficiency, such as those with primary

immunodeficiency disorders or undergoing immunosuppressive therapy (e.g., chemotherapy,
high-dose corticosteroids, organ transplantation), may not be able to receive live attenuated
vaccines. These vaccines contain weakened forms of the pathogen and could pose a risk of
causing disease in individuals with compromised immune systems. However, inactivated or
subunit vaccines are generally considered safe for individuals with immunodeficiency.

3. Pregnancy: Some vaccines may not be recommended during pregnancy due to limited safety
data. Live vaccines, such as measles, mumps, rubella (MMR), and varicella (chickenpox) vaccines,
are generally avoided during pregnancy because of the theoretical risk to the developing fetus.
Inactivated or subunit vaccines, like the influenza vaccine, may be recommended for pregnant
women to protect both the mother and the unborn child.

4. Severe Acute Illness: If a person has a severe acute illness with high fever or is significantly
unwell, vaccination may be delayed until they have recovered. Vaccination is generally
postponed to avoid potential complications or confounding of symptoms related to the illness.

5. History of Guillain-Barré Syndrome (GBS): In some cases, a history of Guillain-Barré Syndrome

may be a precaution or contraindication for certain vaccines. For example, there is a possible
association between GBS and the influenza vaccine, although the risk is rare.

It's important to note that these recommendations may vary depending on the specific vaccine and the
guidelines of the country or region. It is always advisable to consult with healthcare professionals, such
as doctors or immunization specialists, for personalized recommendations based on individual health
conditions and circumstances.

52. Write down the effector mechanisms triggered by vaccine .

Vaccines trigger various effector mechanisms within the immune system to provide protection against
specific pathogens.

Here are some of the key effector mechanisms that vaccines can activate:

1. Antibody Production: Vaccines stimulate the production of specific antibodies by B cells. Antibodies
are proteins that can recognize and bind to the antigens present on the surface of pathogens, marking
them for destruction. Antibodies can neutralize pathogens, prevent their entry into cells, and enhance
other immune responses, such as complement activation and antibody-dependent cell-mediated
cytotoxicity (ADCC).

2. Cell-Mediated Immunity: Vaccines can elicit cell-mediated immune responses involving T cells,
particularly CD4+ helper T cells and CD8+ cytotoxic T cells. CD4+ T cells help activate and regulate other
immune cells, including B cells and cytotoxic T cells, through cytokine production. CD8+ T cells directly
recognize and kill infected cells or tumor cells.

3. Memory Response: Vaccines induce the formation of immunological memory, which is crucial for long-
term protection against future infections. Memory B cells and memory T cells are generated during the
immune response to vaccines. These memory cells "remember" the specific antigen encountered during
vaccination and can mount a rapid and robust immune response upon re-exposure to the pathogen.

4. Cytokine Release: Vaccines can trigger the release of cytokines, which are signaling molecules that
regulate immune responses. Cytokines help orchestrate the recruitment and activation of immune cells,
modulate inflammation, and promote an effective immune response against the pathogen targeted by
the vaccine.

5. Innate Immune Activation: Vaccines can activate the innate immune system, which provides an
immediate and nonspecific defense against pathogens. Innate immune cells, such as dendritic cells,
macrophages, and natural killer cells, recognize and respond to vaccine components. This activation
facilitates the initiation of adaptive immune responses and enhances the overall immune response.

6. Targeted Elimination of Pathogens: Vaccines can stimulate the immune system to specifically recognize
and eliminate the pathogen targeted by the vaccine. This can involve direct killing of pathogens by
immune cells, such as phagocytosis by macrophages or cell lysis by cytotoxic T cells, or the indirect
action of antibodies that bind to and neutralize pathogens.

Overall, vaccines aim to mimic the natural immune response to a pathogen by activating various effector
mechanisms. These mechanisms collectively work to eliminate the pathogen, prevent infection or
disease, and establish long-lasting immune memory to provide protection against future encounters with
the targeted pathogen.
53. Describe the extrafollicular and germinal center responses to protein antigen after vaccination.

After vaccination with a protein antigen, the immune system initiates both extrafollicular and germinal
center responses. Here's a description of these two responses:

1. Extrafollicular Response: The extrafollicular response is an early and rapid immune response that
occurs outside the germinal centers of lymphoid tissues, such as lymph nodes and spleen. It is
characterized by the differentiation of B cells into short-lived plasma cells that produce antibodies
against the protein antigen. This response occurs within days of vaccination.

During the extrafollicular response, antigen-presenting cells (APCs) capture the protein antigen and
present it to B cells. The B cells then undergo clonal expansion and differentiation into plasma cells.
These plasma cells secrete large amounts of antibodies, primarily of the IgM class, which provide
immediate protection against the antigen.

The extrafollicular response is essential for early immune defense, but the antibodies produced are of
lower affinity and do not undergo significant affinity maturation. Therefore, this response alone may not
provide long-term protection against the antigen.

2. Germinal Center Response: The germinal center response is a more prolonged and complex process
that occurs within the germinal centers of secondary lymphoid tissues. It typically develops a few days to
weeks after vaccination. The germinal centers are specialized microenvironments where B cells undergo
clonal expansion, somatic hypermutation, and affinity maturation.

Within the germinal centers, B cells that have encountered the protein antigen undergo rounds of
division and genetic recombination, leading to the generation of B cell clones with increased affinity for
the antigen. This process is facilitated by interactions with follicular helper T cells (Tfh cells) and signals
from cytokines and co-stimulatory molecules.

The B cells that acquire higher affinity antigen receptors undergo positive selection, leading to the
differentiation of some cells into long-lived plasma cells that continue to produce high-affinity
antibodies. Other B cells undergo class switching, resulting in the production of antibodies of different
isotypes, such as IgG, IgA, or IgE, with enhanced effector functions.

In addition to plasma cell differentiation, the germinal center response also generates memory B cells.
Memory B cells possess long-term immune memory and can quickly mount an enhanced response upon
re-exposure to the same protein antigen. This memory response is crucial for providing long-lasting
protection against future infections.

In summary, the extrafollicular response provides an initial rapid antibody response, while the germinal
center response generates higher affinity antibodies, long-lived plasma cells, and memory B cells.
Together, these responses contribute to the development of a robust and long-lasting immune response
against the protein antigen after vaccination.

54. Give a comparison between attenuated and inactivated vaccines .

Here is a table that summarizes the key differences between attenuated and inactivated vaccines:

Vaccine type Method of production Ability to replicate Ability to cause disease

Attenuated vaccine Live virus that has been weakened Yes No

Inactivated vaccine Killed virus No No

Attenuated vaccines and inactivated vaccines are two different types of vaccines with distinct
characteristics and mechanisms of action. Here's a comparison between attenuated and inactivated
vaccines:

Attenuated Vaccines:

1. Definition: Attenuated vaccines are made from live viruses or bacteria that have been weakened or
attenuated through laboratory processes.

2. Pathogen Viability: Attenuated vaccines contain live but weakened forms of the pathogen.

3. Immune Response: Attenuated vaccines replicate within the body, resembling natural infections, and
stimulate both humoral (antibody-mediated) and cellular immune responses.

4. Duration of Immunity: Attenuated vaccines often provide long-lasting immunity, sometimes even
lifelong, as they elicit robust and durable immune responses.

5. Single Dose: Attenuated vaccines generally require fewer doses, often a single dose or a few doses, to
establish immunity.

6. Side Effects: Attenuated vaccines can cause mild symptoms similar to the natural infection, but severe
adverse reactions are rare.

7. Examples: Measles, mumps, rubella (MMR), oral polio vaccine (OPV), yellow fever vaccine, varicella
(chickenpox) vaccine.
Inactivated Vaccines:

1. Definition: Inactivated vaccines are made from pathogens (viruses or bacteria) that have been killed or
inactivated through physical or chemical methods.

2. Pathogen Viability: Inactivated vaccines contain pathogens that have been rendered non-viable,
meaning they cannot replicate or cause disease.

3. Immune Response: Inactivated vaccines primarily stimulate humoral immune responses, leading to
the production of specific antibodies.

4. Duration of Immunity: Inactivated vaccines may require booster doses to maintain protective
immunity, as the immune response may wane over time.

5. Multiple Doses: Inactivated vaccines often require multiple doses, usually two or more, to achieve
optimal immunity.

6. Side Effects: Inactivated vaccines generally have fewer side effects compared to attenuated vaccines,
as they do not replicate in the body. Common side effects are mild and transient.

7. Examples: Inactivated polio vaccine (IPV), hepatitis A vaccine, influenza vaccine (injection), pertussis
(whooping cough) vaccine, rabies vaccine.

Overall, attenuated vaccines offer the advantage of closely mimicking natural infections and inducing
strong and long-lasting immune responses. However, they carry a small risk of causing disease in
individuals with weakened immune systems. In contrast, inactivated vaccines are safer but may require
more doses and may provide a more limited immune response. The choice between the two types of
vaccines depends on various factors, including the characteristics of the pathogen, the target population,
safety considerations, and desired immune responses.

4.1 Answer of the Q/A(Suhani mam)

4. characteristics of self and nonself .

5. Fundamental characteristics of MHC molecule

The fundamental characteristics of MHC molecules are:

1. They are cell surface proteins that present antigens to T cells.

2. They are encoded by the major histocompatibility complex (MHC) genes.
3. There are two main classes of MHC molecules: class I and class II.
4. Class I MHC molecules present antigens from inside the cell to CD8+ T cells.
5. Class II MHC molecules present antigens from outside the cell to CD4+ T cells.
6. MHC molecules are highly polymorphic, meaning that there are many different variants of each
MHC gene.
 This polymorphism allows the immune system to distinguish between self and non-self antigens.

MHC molecules are essential for the adaptive immune response, which is the body's ability to recognize
and respond to specific pathogens.

13. The innate immune system does not react against host- explain.

Pattern recognition receptors (PRRs) are proteins that are found on the surface of cells of the innate
immune system. They recognize molecules that are common to pathogens, such as bacteria and viruses.
When a PRR binds to a pathogen, it triggers a series of events that lead to the destruction of the
pathogen.

The innate immune system does not react against the host because PRRs are designed to recognize
molecules that are common to pathogens. These molecules are not found on the surface of healthy cells,
so the innate immune system does not attack them.

Overall, the innate immune system has evolved to recognize and respond to foreign pathogens while
minimizing damage to the host's own cells and tissues. This selective targeting of pathogens is essential
for the immune system to effectively protect the host from infection and disease.

14. How hapten can be used in the study of antigenicity?

Haptens are small molecules that can bind to larger carrier molecules, but cannot themselves elicit an
immune response. When a hapten is conjugated to a carrier molecule, the resulting complex can
function as an antigen and elicit an immune response in the host organism.

Haptens can be used in the study of antigenicity by serving as model antigens to investigate the
molecular basis of antigen recognition by the immune system. By conjugating a hapten to a carrier
protein, researchers can examine how the immune system recognizes and responds to the complex.

Haptens can also be used in the production of antibodies. For example, a hapten-carrier conjugate can
be used to immunize an animal, which will produce antibodies that recognize the hapten portion of the
conjugate. These antibodies can then be used in various immunoassays to detect the presence of the
hapten in biological samples.

Overall, the use of haptens in the study of antigenicity provides a useful tool for investigating the
molecular mechanisms of immune recognition and for developing novel immunodiagnostic and
immunotherapeutic approaches.

15. What are the characteristics and functions of antigen presenting cell?

Antigen presenting cells (APCs) are specialized immune cells that play a critical role in the immune
response by capturing, processing, and presenting antigens to other immune cells. There are several
types of APCs, including dendritic cells, macrophages, and B cells, each with slightly different
characteristics and functions.

Some of the key characteristics of APCs include:

1. Expression of major histocompatibility complex (MHC) molecules: APCs express MHC molecules
on their surface, which enable them to present antigens to T cells.
 2. Expression of co-stimulatory molecules: APCs express co-stimulatory molecules, such as CD80
and CD86, which are required for full activation of T cells.
3. High endocytic activity: APCs have a high capacity for endocytosis, allowing them to capture and
internalize antigens.
4. Mobility: APCs are highly motile and can migrate from peripheral tissues to lymph nodes to
present antigens to T cells.

The functions of APCs include:

1. Antigen presentation: APCs capture and process antigens, and present them to T cells in the
context of MHC molecules.
2. T cell activation: APCs activate T cells by presenting antigen-MHC complexes and co-stimulatory
molecules.
3. Immune regulation: APCs play a critical role in regulating the immune response by promoting
tolerance to self-antigens and preventing autoimmune responses.
4. Cytokine secretion: APCs secrete cytokines that help to direct the immune response and activate
other immune cells.

Overall, APCs are essential components of the immune system that play a critical role in initiating and
directing immune responses. By presenting antigens to T cells and regulating their activation, APCs help
to orchestrate the immune response and maintain immune homeostasis.

17. how phylogenetic distance different species affect antigenic property?

The phylogenetic distance between different species can affect their antigenic properties. As species
diverge, their proteins and other molecules tend to become more different. This can make it more
difficult for the immune system of one species to recognize and respond to the antigens of another
species.

For example, humans and chimpanzees are closely related species, and their immune systems are able to
recognize and respond to each other's antigens. However, humans and mice are more distantly related,
and their immune systems are less able to recognize and respond to each other's antigens.

21. Comparison between hapten and adjuvant.

Haptens and adjuvants are two different types of molecules that can be used in immunological research
and vaccine development.

1. Definition:
A hapten is a small molecule that can bind to a larger molecule to form a complex that can elicit
an immune response, while an adjuvant is a substance that is added to a vaccine to enhance the
immune response to the antigen.
 2. Size and chemical structure:
Haptens are typically small, organic molecules that are not immunogenic on their own but can
elicit an immune response when coupled to a larger molecule. Adjuvants, on the other hand, are
typically larger molecules that can interact with the immune system to enhance the immune
response to an antigen.
3. Mechanism of action:
Haptens function by binding to a larger carrier molecule, which enables them to be recognized
by the immune system and elicit an immune response. Adjuvants, on the other hand, work by
stimulating the innate immune system and enhancing the activation of antigen-presenting cells
(APCs), which in turn leads to a stronger and more sustained adaptive immune response.

4. Applications:
Haptens are often used in research to investigate the molecular basis of antigen recognition by
the immune system or to develop diagnostic assays that detect the presence of specific
molecules in biological samples. Adjuvants are commonly used in vaccine development to
enhance the immunogenicity of antigens and improve the efficacy of the vaccine.

In summary, while haptens and adjuvants are both important tools in immunological research and
vaccine development, they differ in their size, chemical structure, mechanism of action, and applications.
Haptens are small, non-immunogenic molecules that can be coupled to larger molecules to elicit an
immune response, while adjuvants are larger molecules that work by enhancing the immune response to
an antigen.

4.2 Answer of the Q/A(Shilu sir)

7. What is colony stimulating factor?

Colony-stimulating factors (CSFs) are a group of proteins that play an important role in regulating the
production and differentiation of white blood cells (leukocytes) in the bone marrow. They are produced
by a variety of cells in the body, including stromal cells, fibroblasts, and immune cells.

There are several types of CSFs, including granulocyte-colony stimulating factor (G-CSF), macrophage-
colony stimulating factor (M-CSF), and granulocyte-macrophage-colony stimulating factor (GM-CSF),
each of which has specific functions in the regulation of different types of white blood cells.

CSFs act by binding to specific receptors on the surface of hematopoietic stem cells and progenitor cells
in the bone marrow, stimulating their proliferation and differentiation into mature white blood cells. This
process is important for maintaining an adequate supply of functional white blood cells to fight off
infections and maintain immune homeostasis.

In addition to their role in regulating white blood cell production, CSFs have also been used
therapeutically to stimulate the production of white blood cells in patients with compromised immune
systems, such as those undergoing chemotherapy or bone marrow transplantation.
10. Describe the classification and function of t lymphocyte

T lymphocytes, also known as T cells, are a type of white blood cell that play a central role in adaptive
immunity. They are classified into different subsets based on the expression of specific cell surface
molecules and their functions. Here are the main subsets of T lymphocytes and their functions:

1) Helper T Cells (CD4+ T Cells):

Function: Helper T cells play a crucial role in coordinating immune responses by
providing help and activating other immune cells. They recognize antigens presented
by MHC class II molecules on antigen-presenting cells (APCs).
Subsets:
i) Th1 cells: Activate and stimulate cytotoxic T cells to combat intracellular infections,
enhance macrophage function, and promote cell-mediated immune responses.
ii) Th2 cells: Assist B cells in producing antibodies, particularly in response to extracellular
parasites and allergens. They promote humoral immune responses.
2) Cytotoxic T Cells (CD8+ T Cells):
Function: Cytotoxic T cells are primarily responsible for eliminating infected or
abnormal cells. They recognize antigens presented by MHC class I molecules on
infected cells or tumor cells.
i) Activation: Cytotoxic T cells become activated upon recognition of specific antigen-
MHC class I complexes and then release cytotoxic molecules, such as perforin and
granzymes, to induce target cell death.

3) Memory T Cells:
i) Function: Memory T cells are long-lived cells that persist after an initial immune
response and provide rapid and enhanced responses upon re-exposure to the same
antigen. They contribute to immunological memory, allowing the immune system to
respond more effectively to subsequent infections.

These subsets of T lymphocytes work together to mount effective immune responses against pathogens,
control immune reactions, and maintain immune homeostasis. They exhibit specialized functions and
interactions with other immune cells, contributing to the overall diversity and specificity of the immune
system.

Word Bites
1. MHC molecule