Because learning changes everything.

HUMAN BIOLOGY
Seventeenth Edition

Sylvia S. Mader
Michael Windelspecht

Chapter 7
The Lymphatic and
Immune Systems

© McGraw Hill LLC. All rights reserved. No reproduction or distribution without the prior written consent of McGraw Hill LLC.
 7.1 The Lymphatic System 1

Learning Outcomes:
• Describe the structure and function of the lymphatic
system.
• Explain the origins and components of lymph.
• Explain how the lymphatic system interacts with the
circulatory system.

© McGraw Hill LLC 2

 7.1 The Lymphatic System 2

The lymphatic system.

Consists of lymphatic vessels and organs.
Three main functions contributing to homeostasis:
• Lymphatic capillaries absorb excess interstitial fluid and
return it to the bloodstream.
• Lymphatic capillaries absorb fats from the digestive tract
and transport them to the bloodstream.
• Lymphoid organs help to defend the body against disease.
• This function is mainly carried out by the white blood cells present
in lymphatic vessels, lymphoid organs, and the blood.

© McGraw Hill LLC 3

 Lymphatic Vessels 1

Lymphatic vessels.
Carry a fluid called lymph.
Begin as blind-ended lymphatic capillaries in the
tissues.
• As lymph moves away from the tissues, the capillaries
merge into lymphatic vessels and then two lymphatic
ducts: the thoracic duct and the right lymphatic duct.
• The larger thoracic duct collects lymph from the body below the
thorax, the left arm, and the left side of the head and neck and
empties into the left subclavian vein.
• The right lymphatic duct returns lymph from the right arm and right
side of the head and neck into the right subclavian vein.
© McGraw Hill LLC 4
 Organs and Vessels of the Lymphatic
System (Figure 7.1)

Access the text alternative for slide images.

© McGraw Hill LLC 5

 Lymphatic Vessels 2

Lymphatic vessels, continued.

The anatomy of the larger lymphatic vessels is
similar to that of cardiovascular veins, including the
presence of valves.
• Valves prevent lymph from flowing backward.
The movement of lymph is largely dependent on
skeletal muscle contraction.

© McGraw Hill LLC 6

 Lymphatic Organs
Lymphatic organs.
• Two types: primary and secondary.
• Primary lymphatic organs: red bone marrow,
thymus.
• Secondary lymphatic organs: lymph nodes, spleen,
tonsils.

© McGraw Hill LLC 7

 Tissue Structure of the Lymphatic Organs
(Figure 7.2)

Access the text alternative for slide images.

© McGraw Hill LLC

(a and b): Ed Reschke/Stone/Getty Images; (c): Ed Reschke; (d): Alvin Telser/McGraw Hill 8
 The Primary Lymphatic Organs 1

Red bone marrow.

• The site of blood cell production.
• In children, most bones have red marrow; only a few
do in adults.
• B cells (B lymphocytes) mature here.

© McGraw Hill LLC 9

 The Primary Lymphatic Organs 2

Thymus.
Bilobed; in the thoracic cavity superior to the heart.
It is largest in children and shrinks as we age.
Two functions:
• Produces thymosin, a hormone that induces the
maturation of T cells (T lymphocytes).
• Immature T cells move from the marrow to the thymus,
where they mature.

© McGraw Hill LLC 10

 The Secondary Lymphatic Organs 1

Spleen.
Filters blood.
In the upper left region of the abdominal cavity.
Connective tissue divides it into white pulp and red
pulp.
• Macrophages in red pulp remove pathogens, debris, and
worn-out red blood cells from the blood.
Has a thin outer capsule, so can rupture from
trauma.

© McGraw Hill LLC 11

 The Secondary Lymphatic Organs 2

Lymph nodes.
Found along the lymphatic vessels.
Filter lymph.
Connective tissue forms a capsule around it and divides it into
compartments.
Filled with macrophages that engulf pathogens and debris.
• Also houses lymphocytes, which fight infections and cancer cells.
Named for their location.
• Axillary nodes are in the armpits; inguinal nodes are in the groin.
Common in the neck, armpit, and groin.
© McGraw Hill LLC 12
 The Secondary Lymphatic Organs 3

Lymphatic nodules.
• Concentrations of lymphoid tissue that don’t have a
capsule.
Tonsils are located in the pharynx.
• Have the same function as lymph nodes; fight
infections that come in through the nose and mouth.
Peyer patches.
• Found in the intestinal walls and the appendix.
• Fight infections that come in via the digestive tract.
© McGraw Hill LLC 13
 Check Your Progress 7.1
Describe how the lymphatic system assists in
fluid homeostasis for the body.
List the primary and secondary lymphatic
organs.
Explain the link between the lymphatic and
circulatory systems.

© McGraw Hill LLC 14

 7.2 Innate Immune Defenses 1

Learning Outcomes:
• List examples of the body’s innate defenses.
• Summarize the events in the inflammatory
response.
• Explain the role of the complement system.

© McGraw Hill LLC 15

 7.2 Innate Immune Defenses 2

Immunity—killing or removing foreign

substances, pathogens, and cancer cells from
the body.
There are two branches of our immune system:
innate and adaptive.
• Innate—fully functional without previous exposure
to a pathogen.
• Adaptive—is initiated when exposed to a pathogen.

© McGraw Hill LLC 16

 7.2 Innate Immune Defenses 3

Innate (nonspecific) immune defenses include:

• Physical and chemical barriers.
• The inflammatory response.
• Protective proteins.

Innate defenses have no recognition of a

pathogen, and no memory.

© McGraw Hill LLC 17

 Overview of Innate Immune Defenses
(Figure 7.3)

© McGraw Hill LLC 18

 Physical and Chemical Barriers 1

First line of defense against pathogens.

Barriers to entry: physical and chemical.
• Physical: skin and mucous membranes.
• The skin has lots of keratin, so is tough; also, exfoliation carries
microbes away from the body.
• Mucous membranes have ciliated cells; the cilia sweep away
mucus with entrapped pathogens.
• Chemical:
• Acidic secretions of sebaceous glands weaken, kill bacteria on the
skin.
• Sweat, saliva, and tears have lysozyme—an antibacterial enzyme.

© McGraw Hill LLC 19

 Physical and Chemical Barriers 2

First line of defense, continued.

Chemical barriers, continued.
• The acidic pH of the stomach inhibits or kills
bacteria.
• Normal flora (microbes that usually reside in the
mouth and intestine) prevent potential pathogens
from taking up residence.
• Chronic use of antibiotics can make one susceptible to
infection by killing off the normal flora.

© McGraw Hill LLC 20

 Inflammatory Response 1

Inflammatory response.
Second line of defense against pathogens.
Employs mainly neutrophils and macrophages to
engulf pathogens.
Four hallmark symptoms: redness, heat, swelling,
and pain.
• Chemicals such as histamine, released by damaged tissue
cells and mast cells, cause the capillaries to dilate and
become more permeable.

© McGraw Hill LLC 21

 Steps of the Inflammatory Response
(Figure 7.4)

Access the text alternative for slide images.

© McGraw Hill LLC 22

 Inflammatory Response 2

Inflammatory response, continued.

Four hallmark symptoms: redness, heat, swelling,
and pain, continued.
• Excess blood flow causes the skin to redden and become
warm.
• Increased temperature inhibits growth of pathogens.
• Increased blood flow brings white blood cells to the area.

© McGraw Hill LLC 23

 Inflammatory Response 3

Inflammatory response, concluded.

• Increased permeability of capillaries allows fluids
and proteins to escape into the tissues.
• Blood clot prevents blood loss.
• Excess fluid in the area (swelling) presses on nerve
endings, causing pain.

© McGraw Hill LLC 24

 Inflammatory Response 4

Inflammatory response, continued.

WBCs move out of the bloodstream into the
surrounding tissue.
• Neutrophils are first; they phagocytize debris, dead cells,
and bacteria.
• Can usually localize any infection and keep it from spreading.
• If die off in great quantities, they become a yellow-white
substance called pus.

© McGraw Hill LLC 25

 Inflammatory Response 5

Inflammatory response, continued.

If neutrophils become overwhelmed, they secrete
cytokines—chemicals that attract more WBCs.
• Monocytes that come to the area become macrophages
—powerful phagocytes.

© McGraw Hill LLC 26

 Protective Proteins 1

Protective proteins.
Complement system—several plasma proteins
designated by the letter C and a number.
• Are involved in and amplify the inflammatory response.
• Some bind to mast cells, triggering histamine release.
• Others attract phagocytes to the scene.
• Some form a membrane attack complex that produces
holes in the surface of bacteria; fluids enter the bacterial
cells and they burst.

© McGraw Hill LLC 27

 Action of the Complement System
(Figure 7.5)

© McGraw Hill LLC 28

 Protective Proteins 2

Protective proteins, continued.

Interferons.
• Chemicals produced by cells that are infected with viruses
as a warning to other cells.
• Bind to receptors of noninfected cells, causing them to
produce substances that interfere with viral replication.

© McGraw Hill LLC 29

 Check Your Progress 7.2
List some examples of the body’s innate
defenses.
Describe the blood cells associated with innate
defenses, and detail how they function.
Discuss the role of complement proteins in
immunity.

© McGraw Hill LLC 30

 7.3 Adaptive Immune Defenses 1

Learning Outcomes:
• Explain the role of an antigen in the adaptive
defenses.
• Summarize the process of antibody-mediated
immunity and list the cells involved in the process.
• Summarize the process of cell-mediated immunity
and list the cells involved in the process.

© McGraw Hill LLC 31

 7.3 Adaptive Immune Defenses 2

Adaptive defenses.
• Come into play when innate (nonspecific) defenses
have failed to prevent an infection.
• Overcome an infection by doing away with the
particular disease-causing agent that has entered
the body.
• Establishes a mechanism for the immune system to
"remember" the action.
• Provide some protection against cancer.

© McGraw Hill LLC 32

 How Adaptive Defenses Work 1

Adaptive defenses, continued.

Respond to antigens (immune system recognizes as
foreign).
• Fragments of bacteria, viruses, molds, and parasitic
worms can all be antigenic.

Abnormal plasma membrane proteins produced by

cancer cells may also be antigens.
The immune system is able to distinguish “self” (our
cells) from “nonself” (pathogens).

© McGraw Hill LLC 33

 How Adaptive Defenses Work 2

Adaptive defenses, concluded.

Depend on the action of B cells (B lymphocytes) or
T cells (T lymphocytes).
B cells and T cells have specific antigen receptors
(plasma membrane proteins that bind to particular
antigens).
• Each lymphocyte has only one type of receptor.
• The receptor and antigen fit together like a lock and key.

© McGraw Hill LLC 34

 How Adaptive Defenses Work 3

There are two pathways of adaptive immunity:

cell-mediated and antibody-mediated.
• In cell-mediated immunity, T cells kill any cells that
are presenting a specific “foreign” antigen.
• In antibody-mediated immunity (also called
humoral immunity), B cells produce antibodies that
bind to free antigens in body fluids.

© McGraw Hill LLC 35

 Overview of Adaptive Immune Defenses
(Figure 7.6)

Access the text alternative for slide images.

© McGraw Hill LLC 36

 B Cells and Antibody-Mediated Immunity
B-cell receptors (BCR)—protein receptors on B
cells.
• An antigen binds to the BCR on only one type of B
cell.
• That one B cell then produces copies of itself—this
group of identical B cells is called a clone.

© McGraw Hill LLC 37

 B-Cell Clonal Selection (Figure 7.7)

Access the text alternative for slide images.

© McGraw Hill LLC 38

 Characteristics of B Cells
• Responsible for antibody-mediated immunity
against pathogens.
• Produced and mature in bone marrow.
• Directly recognize antigen and then undergo
clonal selection.
• Clonal expansion produces antibody-
secreting plasma cells, as well as memory B
cells.

© McGraw Hill LLC 39

 B Cells Become Plasma Cells and Memory
B Cells 1

During clonal expansion, cytokines secreted by

helper T (TH) cells stimulate B cells to clone.
Most of the cloned B cells become plasma cells,
which produce large numbers of antibodies that
bind to the antigen that initiated this whole process.
Some B cells become memory cells, which become
active in future encounters of this same antigen.
• Confer immunity to that antigen.

© McGraw Hill LLC 40

 B Cells Become Plasma Cells and Memory
B Cells 2

After an infection has been overcome, the

plasma cells are no longer needed, so undergo
apoptosis.
• Programmed cell death.

© McGraw Hill LLC 41

 Structure of an Antibody 1

Structure of an antibody.
Y-shaped protein with two arms.
• Each arm has a “heavy” (long) polypeptide chain and a
“light” (short) polypeptide chain.
• These chains have constant regions, located at the trunk of the Y,
where the sequence of amino acids is fixed.
• Antibodies are classified by the structure of its constant region.

© McGraw Hill LLC 42

 The Structure of an Antibody (Figure 7.8)

Access the text alternative for slide images.

© McGraw Hill LLC

(b): Dr. Arthur J. Olson 43
 Structure of an Antibody 2

Structure of an antibody, continued.

The variable regions form an antigen-binding site;
their shape is specific to a particular antigen.
• The antigen combines with the antibody at the antigen-
binding site in a lock-and-key manner.

© McGraw Hill LLC 44

 Structure of an Antibody 3

Structure of an antibody, concluded.

• Antibodies may consist of single Y-shaped
molecules, called monomers, or may be paired
together in a dimer.
• Some are pentamers—clusters of five Y-shaped
molecules linked together.

© McGraw Hill LLC 45

 Structure of an Antibody 4

Neutralization—antibodies coat viruses and

toxins completely, “neutralizing” them and
removing the threat.
Immune complex—a clump of antigens combined
with antibodies.
• The immune complex attracts WBCs.

© McGraw Hill LLC 46

 Classes of Antibodies 1

Classes of antibodies.
There are five classes of circulating antibodies: IgG,
IgM, IgA, IgD, IgE.
IgG—the major type in blood; smaller numbers are
found in lymph and interstitial fluid.
• Bind to pathogens, toxins.
• Crosses the placenta from mother to fetus; confers
temporary immune protection.

© McGraw Hill LLC 47

 Classes of Antibodies (Table 7.1)
Table 7.1 Classes of Antibodies
Class Presence Function
IgG Main antibody type in circulation; Binds to pathogens, activates
crosses the placenta from mother to complement, and enhances
fetus phagocytosis by white blood cells

IgM Antibody type found in circulation; Activates complement and clumps

largest antibody; first antibody cells
formed by a newborn; first antibody
formed with any new infection

IgA Main antibody type in secretions Prevents pathogens from attaching

such as saliva and breast milk to epithelial cells in digestive and
respiratory tracts

IgD Antibody type found on surface of Signifies readiness of B cell

immature B cells
IgE Antibody type found as antigen Responsible for immediate allergic
receptors on mast cells in tissues response and protection against
certain parasitic worms

© McGraw Hill LLC 48

 Classes of Antibodies 2

Classes of antibodies, continued.

IgM—pentamers; the first antibodies produced by a
newborn.
• The first to appear in blood after an infection begins and
the first to disappear when the infection is over.
• Activate the complement system.

© McGraw Hill LLC 49

 Classes of Antibodies 3

Classes of antibodies, concluded.

IgA—monomers or dimers containing two Y-shaped
structures.
• Main type of antibody found in body secretions: saliva,
tears, mucus, and breast milk.
• Bind to pathogens so they can’t reach the bloodstream.
IgD—antigen receptors on immature B cells.
IgE—prevent parasitic worm infections.
• Can also cause allergic responses.

© McGraw Hill LLC 50

 Monoclonal Antibodies
Monoclonal antibodies.
• All are identical and are produced by plasma cells
derived from the same B cell.
• Can be produced in the lab.
• Are used for medical tests and treatments.

© McGraw Hill LLC 51

 The Production of Monoclonal Antibodies
(Figure 7.9)

Access the text alternative for slide images.

© McGraw Hill LLC 52

 T Cells and Cell-Mediated Immunity 1

How T Cells Recognize an Antigen.

T-cell receptor (TCR)—unique receptor on the
surface of each T cell.
• B cells also have unique receptors, but unlike B cells, T
cells are unable to recognize an antigen without help; it
must be displayed to them by an antigen-presenting cell
(APC) such as a macrophage.
• After phagocytizing a pathogen, APCs travel to the T cells
in a lymph node or the spleen.

© McGraw Hill LLC 53

 T Cells and Cell-Mediated Immunity 2

How T Cells Recognize an Antigen, continued.

• APCs break the ingested pathogen apart in a
lysosome.
• A piece of the pathogen is then displayed in the
groove of a major histocompatibility complex
(MHC) protein on the cell’s surface. The two classes
of MHC proteins are called MHC I and MHC II.

© McGraw Hill LLC 54

 T Cells and Cell-Mediated Immunity 3

How T Cells Recognize an Antigen, continued.

Human MHC II proteins are called human leukocyte
antigens (HLAs).
• Found on all body cells.
• There are three general groups of HLAs (HLA-A, HLA-B,
and HLA-DR), each with a number of protein variations.
• Each person has a unique combination of HLAs.
• HLAs of identical twins, however, are identical.

© McGraw Hill LLC 55

 Clonal Expansion 1

Clonal Expansion.
Many copies of the activated T cell are produced.
Occurs when a macrophage presents an antigen to a
T cell that has the specific TCR that will bind this
particular antigen.
• This activates the T cell, causing it to undergo clonal
expansion.
Some T cells become cytotoxic T cells, and some will
become helper T cells.

© McGraw Hill LLC 56

 The Clonal Selection Model for T Cells
(Figure 7.10)

Access the text alternative for slide images.

© McGraw Hill LLC 57

 Clonal Expansion 2

Cytotoxic T cell.
Has storage vacuoles that contain perforins and
enzymes called granzymes.
After binding to a virus-infected cell or tumor cell, it
releases perforins, which punch holes in the plasma
membrane, forming a pore.
• Cytotoxic T cells then deliver granzymes into the pore,
causing the cell to undergo apoptosis.
Responsible for cell-mediated immunity.

© McGraw Hill LLC 58

 How Cytotoxic T Cells Kill Infected Cells
(Figure 7.11a) 1

Access the text alternative for slide images.

© McGraw Hill LLC 59

 How Cytotoxic T Cells Kill Infected Cells
(Figure 7.11b) 2

© McGraw Hill LLC

(b): Steve Gschmeissner/Science Source 60
 Clonal Expansion 3

Helper T cells.
• Secrete cytokines that enhance the response of all
types of immune cells.
• B cells cannot be activated without T-cell help.
• The human immunodeficiency virus (HIV), which
causes AIDS, infects helper T cells, thus inactivating
the immune response.

© McGraw Hill LLC 61

 Characteristics of T Cells
• Cell-mediated immunity against virus-infected
cells and cancer cells.
• Produced in bone marrow, mature in thymus.
• Cytotoxic T cells destroy nonself antigen-
bearing cells.
• Helper T cells secrete cytokines that control
the immune response.

© McGraw Hill LLC 62

 Check Your Progress 7.3
Detail how innate defense differs from adaptive
defense.
Distinguish between the cells involved in
targeting an antigen present within a cell of the
body versus an antigen free in the interstitial
fluid.
Explain how memory lymphocytes are formed
and state their function.

© McGraw Hill LLC 63

 7.4 Acquired Immunity 1

Learning Outcomes:
• Distinguish between active and passive immunity.
• Recognize the importance of cytokines in immunity.

© McGraw Hill LLC 64

 7.4 Acquired Immunity 2

Immunity.
• Can be brought about naturally through an infection
or artificially through medical intervention.
• There are 2 types of acquired immunity: active and
passive.

© McGraw Hill LLC 65

 Active immunity
Active immunity.
The individual’s body makes antibodies against a particular
antigen.
Can happen through natural infection or through
immunization involving vaccines.
• Contain antigens from the pathogen or the pathogens themselves
(treated so they can no longer cause disease).
The first exposure to an antigen produces a primary
response; second exposure a secondary response.
• Depends on memory lymphocytes and sometimes booster shots.

© McGraw Hill LLC 66

 How Immunizations Cause Active
Immunity (Figure 7.12)

Access the text alternative for slide images.

© McGraw Hill LLC 67

 Passive Immunity
Passive immunity.
An individual is given antibodies to combat a
disease; since not produced by the individual’s
plasma cells, passive immunity is temporary.
That is, newborn infants are passively immune to
some diseases because IgG antibodies have crossed
the placenta from the mother’s blood.
• Breast-feeding prolongs this natural passive immunity
because IgG and IgA antibodies are present in mother’s
milk.
That is, can also receive antibodies by injection.
© McGraw Hill LLC 68
 Delivery Mechanisms of Passive Immunity
(Figure 7.13)

Access the text alternative for slide images.

© McGraw Hill LLC

(b): JGI/Blend Images; (c): Luis Alvarez/DigitalVision/Getty Images 69
 Cytokines and Immunity
Cytokines—signaling molecules produced by T
lymphocytes, macrophages, and other cells.
• Regulate WBC formation and/or function.
• That is, interferon and interleukins are cytokines and
are used in various medical treatments.

© McGraw Hill LLC 70

 Check Your Progress 7.4
Define acquired immunity and give some
examples.
Describe how passive immunity is developed.
Compare the two types of immune therapies that
can assist passive immunity.

© McGraw Hill LLC 71

 7.5 Disorders of the Immune System
Learning Outcomes:
• Explain the relationship between AIDS and
opportunistic infections.
• Summarize how the HIV virus is transmitted and the
methods by which AIDS is treated.
• Explain what causes an allergic reaction.
• Identify the effects of autoimmune diseases on the
body.

© McGraw Hill LLC 72

 HIV and AIDS 1

The human immunodeficiency virus (HIV)

causes acquired immunodeficiency syndrome
(AIDS).
Two main types of HIV: HIV-1 (the more
widespread, virulent form) and HIV-2.
HIV-2 found in the green monkey, lives in western Africa.
HIV-1 replica virus found in a subgroup of chimpanzees once
common in west-central Africa.
• This suggests that HIV viruses originated in nonhuman primates, then
mutated to HIV after humans ate nonhuman primate meat.

© McGraw Hill LLC 73

 HIV and AIDS 2

HIV.
Can infect cells with particular surface receptors.
Infects and destroys cells of the immune system.
• That is, helper T cells and macrophages.
The body’s ability to fight an infection declines as
the number of helper T cells declines.
• A person becomes ill with various diseases.

© McGraw Hill LLC 74

 HIV and AIDS 3

AIDS.
• The advanced stage of HIV infection.
• Person develops one or more of many opportunistic
infections.
Opportunistic infection—one that has the
opportunity to occur only because the immune
system is severely weakened.

© McGraw Hill LLC 75

 Stages of an HIV Infection (Figure 7.14)

Access the text alternative for slide images.

© McGraw Hill LLC 76

 Transmission and Prevention of HIV 1

HIV transmission modes:

• Sexual contact with a person with HIV (vaginal or
rectal intercourse and oral-genital contact); most
common.
• Needle sharing among people who use IV drugs.
• Transfusions of infected blood or blood-clotting
factors; very rare.
• Babies born to women with HIV; before or during
birth or through breast-feeding.

© McGraw Hill LLC 77

 Transmission and Prevention of HIV 2

Transmission, continued.
Body fluids with the highest concentrations of HIV:
blood, semen, vaginal fluid, breast milk.
HIV is not transmitted through:
• Contact in the workplace, schools, or social settings.
• Kissing, hugging, or shaking hands.
• Touching toilet seats, doorknobs, dishes, drinking glasses,
food, or pets.

© McGraw Hill LLC 78

 Transmission and Prevention of HIV 3

Prevention.
• Prevention strategies needed to fight the spread of
HIV differ worldwide due to differences in cultures,
sexual practices, and belief systems.
• The general message of HIV prevention is
abstinence, sex with only one uninfected partner, or
consistent use of a condom during sexual
encounters.

© McGraw Hill LLC 79

 HIV Treatment 1

Treatment.
There is no cure for AIDS yet.
Individuals immediately undergo antiviral treatment
following a positive HIV test result.
Highly active antiretroviral therapy (HAART) usually
can stop HIV replication; viral load becomes
undetectable.
• HAART uses a combination of drugs that interfere with the
life cycle of HIV.
• When HAART is discontinued, the virus rebounds.
© McGraw Hill LLC 80
 HIV Treatment 2

Treatment, continued.
Possible drug combinations:
• Entry inhibitors stop HIV from entering a cell. The virus is prevented
from binding to a receptor in the plasma membrane.
• Reverse transcriptase inhibitors, such as zidovudine (AZT), interfere
with the operation of the reverse transcriptase enzyme.
• Integrase inhibitors prevent HIV from inserting its genetic material into
that of the host cells.
• Protease inhibitors prevent protease from cutting up newly created
polypeptides.
• Assembly and budding inhibitors are in the experimental stage, and
none are available as yet.

© McGraw Hill LLC 81

 HIV Treatment 3

Treatment, continued.
Over 21 million people worldwide are now receiving
HIV treatment.
Drug therapy dangers:
• People with HIV may become lax in their efforts to avoid
infection, knowing that drug therapy is available.
• Drug use leads to drug-resistant viruses.
• Some HIV viruses have become drug-resistant when patients
failed to adhere to their drug regimens.

© McGraw Hill LLC 82

 Hypersensitivity Reactions
Hypersensitivity reactions—when the immune
system overreacts and causes harm to the body.
• That is, allergies, receiving an incompatible blood
type, tissue rejection, or autoimmune disease.

© McGraw Hill LLC 83

 Allergies 1

Allergies.
Hypersensitivity to allergens such as pollen, food, or animal
hair, which would normally be harmless.
Immediate allergic response—occurs within seconds of
contact with the antigen.
• Caused by IgE antibodies attached to receptors on mast cells and
basophils, which release histamine when they bind allergens.
• When pollen is an allergen, histamine stimulates the mucous
membranes of the nose and eyes to release fluid (runny nose and
watery eyes—hay fever).
• With asthma, airways constrict, resulting in wheezing.
• Food allergies—nausea, vomiting, diarrhea.
© McGraw Hill LLC 84
 Allergies 2

Allergies, continued.
Anaphylactic shock—an immediate allergic response.
• Occurs when the allergen enters the bloodstream.
• Characterized by a sudden and life-threatening drop in
blood pressure due to increased permeability of the
capillaries by histamine.
• Taking epinephrine can counteract this reaction.
Delayed allergic responses—initiated by memory T
cells at the location of contact with the allergen.
• That is, poison ivy.
© McGraw Hill LLC 85
 Other Immune Problems 1

Rejection of transplanted tissue.

The recipient’s immune system recognizes that
the transplanted tissue is not “self.”
Cytotoxic T cells attack the transplanted tissue.
Can be controlled with immunosuppressive drugs
and by transplanting organs that have the same MHC
proteins in the donor and recipient.
• Some immunosuppressive drugs act by inhibiting the
production of cytokines.

© McGraw Hill LLC 86

 Other Immune Problems 2

Rejection of transplanted tissue, continued.

• Xenotransplantation—transplanting organs from an
animal.
• Some organs can be grown in a lab.

© McGraw Hill LLC 87

 Other Immune Problems 3

Severe combined immunodeficiency disease.

• Both antibody- and cell-mediated immunity are
inadequate or lacking.
• A minor infection can be fatal.
• Treated with bone marrow transplant or gene
therapy.

© McGraw Hill LLC 88

 Other Immune Problems 4

Acquired immune deficiencies can be caused by

infections, chemical exposure, or radiation.
Acquired immunodeficiency syndrome (AIDS) results
from infection with the human immunodeficiency
virus (HIV).
• AIDS patients are more susceptible to infections and have a
higher risk of cancer.

© McGraw Hill LLC 89

 Other Immune Problems 5

Autoimmune disease.
Cytotoxic T cells or antibodies attack the body’s own
cells as if they were foreign.
Involves both genetic and environmental factors.
Sometimes follows an infection.
• That is, rheumatic fever—antibodies induced by a
streptococcal bacterial infection of the throat also react
with heart muscle.
• Damages the heart muscle and valves.
• That is, rheumatoid arthritis—antibodies against joints.
© McGraw Hill LLC 90
 Rheumatoid Arthritis (Figure 7.15)

© McGraw Hill LLC

lathuric/iStock/Getty Images 91
 Other Immune Problems 6

Systemic lupus erythematosus (SLE).

Usually just called “lupus.”
Various symptoms: facial rash, fever, joint pain.
Damage to the central nervous system, heart, and
kidneys can be fatal.
Produce high levels of anti-DNA antibodies.
• All human cells (except red blood cells) contain DNA, so
the symptoms of lupus can be exhibited throughout the
body.

© McGraw Hill LLC 92

 Other Immune Problems 7

Myasthenia gravis.
• Antibodies attach to and interfere with the function
of muscles.
• The result is severe muscle weakness, eventually
resulting in death from respiratory failure.

© McGraw Hill LLC 93

 Other Immune Problems 8

Multiple sclerosis.
• T cells attack the myelin sheath covering nerve
fibers, causing central nervous system dysfunction,
double vision, and muscular weakness.
• MS may not be an autoimmune disease, because a
specific antigen has not been identified.
• Treatments for all of these diseases are drugs
designed to decrease the immune response.

© McGraw Hill LLC 94

 Check Your Progress 7.5
Define the types of complications and disorders
associated with the functioning of the immune
system.
Detail how an antibody works during an allergic
reaction.
Hypothesize why an autoimmune disorder
sometimes develops after an infection.

© McGraw Hill LLC 95

 End of Main Content

Because learning changes everything. ®

www.mheducation.com

© McGraw Hill LLC. All rights reserved. No reproduction or distribution without the prior written consent of McGraw Hill LLC.