Mycopathologia (2007) 164:57–64

DOI 10.1007/s11046-007-9026-7

Review of innate and specific immunity in plants and

animals
Marcello Iriti Æ Franco Faoro

Received: 19 March 2007 / Accepted: 9 May 2007 / Published online: 7 June 2007
Ó Springer Science+Business Media B.V. 2007

Abstract Innate immunity represents a trait com- terms of fitness costs of induced resistance and
mon to plants and animals, based on the recognition autotoxicity. A set of similar defence responses
of pathogen associated molecular patterns (PAMPs) shared from plants and animals, such as defensins,
by the host pattern recognition receptors (PRRs). It is reactive oxygen species (ROS), oxylipins and pro-
generally assumed that a pathogen strain, or race, grammed cell death (PCD) are briefly described.
may have elaborated mechanisms to suppress, or
evade, the PAMP-triggered immunity. Once this plan Keywords Adaptive immunity
Autoimmunity

was successful, the colonization would have been Autotoxicity
Fitness costs
innate immunity
SAR
counteracted by an adaptive strategy that a plant
cultivar must have evolved as a second line of
defence. In this co-evolutionary context, adaptive Introduction
immunity and host resistance (cultivar-pathogen race/
strain-specific) has been differently selected, in Either plants and animals are capable of recognizing
animals and plants respectively, to face specialized and distinguishing between self and non-self. How-
pathogens. Notwithstanding, plant host resistance, ever, some phylogenetically ancient structures and
based on matching between resistance (R) and strategies used in defence have been retained by
avirulence (avr) genes, represents a form of innate parallel evolution, while some others appeared more
immunity, being R proteins similar to PRRs, although recently during phylogenesis [1, 2].
able to recognize specific virulence factors (avr In this context, innate immunity, common to plants
proteins) rather than PAMPs. Besides, despite the and animals, deeply differs from the adaptive one,
lack of adaptive immunity preserved plants from which is restricted to vertebrates. Plants, lacking
autoimmune disorders, inappropriate plant immune immunoglobulin molecules, circulating immune cells
responses may occur, producing some side-effects, in and phagocytic processes, do not possess any adap-
tive immunity, despite an array of innate defence
mechanisms. Innate immunity can be considered as a
M. Iriti (&)
F. Faoro battery of first-line defences against microbes, that
Plant Pathology Institute, University of Milan, pre-exists pathogen challenging and adaptive immu-
Via Celoria 2, Milan 20133, Italy nity triggering in animals [3].
e-mail: [email protected]
Recognition of PAMPs (pathogen associated
M. Iriti
F. Faoro molecular patterns) represents the major trait of
CNR, Plant Virology Institute, U.O. Milan, Italy innate immunity common to plants and animals,

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with the paradigm of drosophila toll receptors, during their entire life cycle, while the latter can live
mammalian TLRs (toll-like receptors) and the on either living and dead hosts and nutrient media,
products of R (resistance) genes in plants, collec- requiring the plant only for a part of their life cycle.
tively termed as pattern recognition receptors In addition, nonobligate parasites include facultative
(PRRs) [4]. Thus, PAMPs, more commonly known saprophytes or facultative parasites (or necrotrophs),
as general elicitors in plants, including lipopolysac- depending on their main habitus, parasitic or sapro-
charides (LPS), peptidoglycans, flagellin, microbial phytic respectively [10].
cell wall fragments, phospholipids, proteins, double With regard to infection process, two different
stranded RNA and methylated DNA, are able to routes exist in animals. The endogenous infection
elicit a host defence response by binding to route pertains to the commensal body flora, depend-
receptors [5]. Besides, innate immunity receptors, ing on overgrowth of fungal strains (i.e. Candida
both in plants and animals, are nonclonal and albicans, Fig. 1a), at the nonsterile sites where they
encoded in the germline, unlike B and T lymphocyte perform their commensalisms, such as stomatogna-
receptors, which are otherwise clonal and rearranged thic system, digestive and respiratory tract and genital
during development following somatic recombina- organs, or following translocation from these sites
tions, in addition to be responsible for immunologic towards body compartments that react to their
memory [6]. presence. Differently, the exogenous infection route
Perhaps, in this scenario, plants avoid the main is due to the entry of saprobes from the environment
harmful side effect of adaptive immunity, that is to the human body, usually through the airways and
autoimmunity, due to abnormalities in self tolerance pulmonary tree [8, 11]. Plant pathogenic fungi show a
and the subsequent immune response to self antigens, rather similar behaviour, invading their hosts after
though plant fitness costs, particularly in conditions entering through epigeous organs (leaves and stem),
of low pathogen pressure, might be somewhat such as rust fungi (Fig. 1b) and downy mildews, or
identified with a sort of autoimmune disease [7]. hypogeous organs (roots), for instance Rhizoctonia
solani [10]. However, a downright endogenous
infection route does not exist, although symbiosis
The host-pathogen interaction between plants and fungi frequently occur. Myco-
rryzhae are mutualistic associations taking place at
In animals, fungi causing mycoses consist of two the root level (rizhosphere), where the fungus profits
classes. The primary pathogens infect healthy non- by the carbohydrates assimilated from the plant, and
compromised individuals, whereas the opportunistic the latter, in return, benefits from the fungal hyphae
fungi cause disease in immunodeficient patients, as to improve its own mineral nutrient uptake by roots.
those receiving immunosuppressive therapy, under- Interestingly, mycorryzhae may elicit plant defence
going bone marrow or solid organ transplantation or mechanisms by releasing chitin or chitosan frag-
with acquired immunodeficiency syndrome (AIDS) ments, sensing as PAMPs from the host perception
[8, 9]. In plants, fungal pathogens can be divided into machinery [12].
obligate and nonobligate parasites. The former, also Nevertheless, another evident divergence, between
known as biotrophs, can growth, develop and mul- the animal and plant kingdom, concerns the different
tiply only in close association with their living host, relevance covered by the fungal diseases in animal

Fig. 1 Pathogenic fungi of

animals and plants; (a)
Candida albicans in human
oral mucosa (Periodic Acid-
Shiff staining) and (b)
Uromyces appendiculatus
in bean leaf parenchyma
(Evans’ blue staining)

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and plant pathology. In the latter, diseases caused by plants recognize glucans, chitin, chitosan, ergosterol,
fungi include the most diffuse and damaging ones, in sphingolipids by means of binding proteins involved
contrast to the minor importance of mycoses among in pathogen perception, signal transduction and
the infectious diseases. immunity [5]. In this short survey, the attention is
focused on some components of the innate immunity
shared by animal and plant world, precisely defen-
The host immune response in plants and animals sins, reactive oxygen species (ROS), oxylipins and
programmed cell death (PCD, Fig. 2).
After pathogen challenging, the immune system
provides protection against the infection spreading. Defensins
In plants, innate immunity is the only way to
counteract the disease progression while in verte- These are basic, small, cysteine-rich peptides (up to
brates adaptive immunity, either humoural or cell- 50 amino-acids with at least two excess positive
mediated, is also triggered. Thus plants apparently charges due to lysine and arginine residues) with a
lack in a part of their immune system able to adapt broad-spectrum antibiotic activity. In animals, they
according to the changeable events [1, 6, 13]. are particularly abundant in granules of leukocytes
At the host-fungus interface, plant/animal surface and epithelia, where they are either constitutive and
barriers firstly oppose to pathogen penetration. Intact induced by infection [17]. In plants, defensins are
cutaneous tissues, mucous membranes and respira- found constitutively in storage organs (seeds) and
tory tract lining fluid prevent the infection in animal peripheral cell layers of generative tissues (reproduc-
world, as well as leaf epicuticular layers, suberized, tive organs, fruits and flowers), besides being
cutinized and lignified epidermal tissues do in plants. induced, in vegetative tissues, following infection or
Nevertheless all these outermost barriers can be wounding [18]. Generally, the activity of these
variously overcome from the pathogenic fungi [14, cationic antimicrobial peptides is related to their
15]. If it occurs, pathogen recognition represents the membranolytic properties. Due to their amphipathic
first step at the onset of the host immune response. In characteristics, animal defensins target microbial
animals, PRRs are involved in recognition of PAMPs membranes, inducing ion-permeable pores in lipid
derived from Candida albicans, Aspergillus fumiga- bilayers [17]. Otherwise, plant defensins alter the
tus, Cryptococcus neoformans, Pneumocystis carinii structural integrity of fungal membranes by interact-
and Saccharomyces cerevisiae. Particularly, TLR2 ing specifically with fungal sphingolipids and induc-
and TLR4 recognize constituents of fungal cell wall ing membrane permeabilization, in turn resulting in
and membrane, such as glucans, mannan, proteins, increased calcium influx, potassium efflux and
glycolipids and yeast zymosan [4, 16]. Similarly, reduced fungal growth [18].

Fig. 2 Defence
mechanisms common to PAMP PAMP
plants and animals; (AOC, Direct toxicity
allene oxide cyclase; AOS,
allene oxide synthase;
COX, cyclooxygenase;
LOX, lipoxygenase; PAMP, PRR ROS, DEFENSINS PRR

pathogen associated
molecular pattern; PCD, A ra c h i do n i c a c i d PCD linole(n)ic acid
programmed cell death;
LOX COX LOX
PRR, pathogen recognition
receptor; ROS, reactive AOS
Leukotrienes
oxygen species)
Prostaglandins, AOC
Thromboxanes
E i co s a n o i d s Octadecanoids/Jasmonates

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ROS via an array of oxygenases, able to catalyze the

incorporation of oxygen atoms into PUFAs. Thus,
The production of reactive oxygen species (ROS) is lipoxygenases consume a molecule of oxygen to
another defence reaction that occurs both in animal initiate the synthesis of leukotrienes in animals,
and plant world. In animals, during inflammation and whereas, in plants, the dioxygenation of a-linolenic
immune response, the activated phagocytic white acid is followed by other two enzymatic steps,
cells (neutrophils, macrophages, monocytes) gener- catalyzed by the Allene Oxide Synthase (AOS) and
ate, in their vacuoles, superoxide radical (O2 ) by a Allene Oxide Cyclase (AOC), leading to jasmonates
NADPH oxidase. This radical species is then trans- synthesis [23] (Fig. 2). Alternatively, cyclooxygen-
formed in other ROS (mainly hydrogen peroxide, ases (COX) converts arachidonic acid to prostaglan-
H2O2, and hydroxyl radical, .OH) involved in direct dins and thromboxanes (collectively named
toxicity towards microbes, in a process known as prostanoids) consuming two molecules of oxygen,
respiratory burst [19]. Similarly, in plant cells, in animals, whereas a pathogen-induced oxidase
oxidative burst occurs as an early defence response. (PIOX), with homology to COX, similarly leads to
A plasma membrane located NADPH oxidase, shar- another class of lipid mediators in plants. Either
ing homology with its mammalian counterpart, jasmonates, or octadecanoids, and prostanoids and
produces .O2 , contributing, in conjunction to other leukotrienes, collectively named eicosanoids, exhibit
ROS, to create a hostile apoplastic (extracellular) similar functions in plants and animals respectively,
environment for the pathogen. Interestingly, any plant particularly as regards defence mechanisms [24].
cell can mount a defence response, as proved, for Octadecanoids are involved both in physiological
instance, by the presence of a NADPH oxidase in processes, such as flowering and fruit ripening, and in
many cell types and tissues and by the competence to host defence response to pathogens, wounding and
synthesize phytoalexins. This would compensate for environmental stresses [25]. Likewise, eicosanoids
the absence of a true immune system, meant as cells, play a major role in the regulation of vascular tone,
tissues and organs deputed to defence. inflammation, infection and exposure to allergens,
Enzymes involved in ROS chemistry are the same foods, drugs and xenobiotics [24].
in all pluricellular eucaryotic organisms. The enzyme
superoxide dismutase (SOD) rapidly convert .O2 to PCD
H2O2, which may form OH in presence of transition
metal ions, according to the Haber–Weiss and Fenton Eukaryotic cells display two different ways to die:
reactions [20]. Nonetheless, the mechanisms involved necrosis and apoptosis, each with own peculiar mor-
in the homeostasis of the cell redox status, including phological and biochemical hallmarks. The former is
non-enzymatic and enzymatic scavengers, differ to an accidental, passive and traumatic death, due to
some extent between the two kingdoms [21]. Any- catastrophic toxic events whereas the latter is a
how, the failure of respiratory burst causes chronic genetically encoded physiological death required for
granulomatous disease, in animals, characterized by tissue and organ differentiation and development [26].
life-threatening pyogenic infections and inflamma- Furthermore, apoptosis, or programmed cell death
tory granulomas, as well as defective oxidative burst (PCD), is a fine regulated active process, also involved
impairs, in plants, the defence response orchestrated in immunity, and whose morphological markers
by ROS [20, 22]. include nuclear condensation and DNA fragmentation,
production of reactive oxygen species, increased ion
Oxylipins leakage, cytochrome c release from mitochondria, and
caspase proteolytic activities [26, 27].
These are metabolites produced by the oxidation of In plants, PCD takes place in an array of condi-
polyunsaturated fatty acids (PUFAs), after their tions: during the development of root-tip cells, in the
discharge from the lipid bilayers due to phospholip- differentiation of tracheal elements and lysigenous
ases. Afterwards, free arachidonic and linole(n)ic aerenchyma, in the endosperm and aleurone layers of
acid, the main PUFAs in the biological membranes of the kernel. Also adverse environmental conditions
animals and plants respectively, undergo oxidation and biotic stresses, namely pollutant and pathogen

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attack, can promote PCD in plant [27]. In fact, the pathogen. It exhibits a tight specificity for foreign
hypersensitive response (HR) that may be triggered at (non-self) elicitors (antigens), being able to distin-
the attempted pathogen penetration site is a type of guish among different, even closely related, patho-
PCD, frequently associated with the induction of gens. Furthermore, adaptive immunity has the
systemic immunity (SAR, systemic acquired resis- ability to respond more vigorously to repeated
tance) [28, 29]. In animal immune system, the main exposure to the same pathogen/antigen (immuno-
role of apoptosis pertain to adaptive immunity, logical memory). The main weapons of this
precisely in the restoration of homeostasis at the immune system are antibodies, secreted by B
end of an immune response, when, after lymphocyte lymphocytes and circulating in the blood (humoural
proliferation (clonal expansion), most of the progeny immunity), and T lymphocytes, able to either
of antigen-stimulated lymphocytes die by apoptosis, destroy directly infected cells or activate phago-
leaving only functionally quiescent memory lympho- cytes to kill pathogens (cell-mediated immunity,
cytes [14]. Otherwise, in animals, premature lysis of Fig. 3) [6].
the infected cells, due to apoptosis, can prevent the As above reported, plants lack adaptive immunity,
complete multiplication of progeny virus if cells die although they developed an alternative strategy to
before virus multiplication, or when infected apopto- fulfil an analogous need to survive from the pathogen
tic cells are phagocytosed by macrophages [30]. challenge. Traditionally, their defence mechanisms
Considering the fundamental role of HR-PCD in can be activated by two distinct classes of elicitors.
plant defence, it seems that, during the evolution, General elicitors, or PAMPs, induce non-host resis-
plants implemented PCD more than animals did, as tance by PRRs-mediated recognition, whereas spe-
an effective direct tool to improve their own defence cific elicitors require a more specific system of
armamentarium. perception, leading to the host cultivar-specific
resistance. Specific elicitors are virulence factors
RNAi encoded by the avirulence (avr) genes of a given
pathogen race or strain, enabling it to overcome the
The RNA interference (RNAi) or post-transcriptional PAMP-triggered immunity. At the opposite side of
gene silencing, based on the recognition and pro- the barricade, cultivars of a given plant evolved a
cessing of non-self double-stranded RNA (dsRNA) is strategy to counteract these specialized pathogens.
a defence mechanism against pathogenic nucleic Therefore, the products of the plant resistance genes
acids [31]. Though this mechanism is conserved in all (R) ensure the perception of pathogen race/strain-
eukaryotes, from the unicellular ones to mammals, it specific avr proteins, and the matching between pairs
seems not be involved in defence against fungal of avr and R gene products, has been emphasized by
pathogens. the gene-for-gene theory. Anyhow, either the host
surveillance strategies, i.e. PAMP-triggered (non-host
resistance) and the avr-induced (host resistance),
Adaptive defence mechanisms regardless of general or specific elicitors, constitute
two forms of the same innate immunity, in plants
In vertebrates, adaptive immunity, also termed (Fig. 3), being both PRRs and R proteins nonclonal
specific or acquired immunity, adapts to a distinct and germline-encoded [32–34].
Innate immunity

Innate Non host

Ba s a l re s i s t a n c e resistance
immunity

Adaptive Host
Sp ec ific immu n ity resistance
immunity

Fig. 3 The two subdivisions of plant innate immunity (non- adaptive immunity, respectively; the difference between basal
host and host resistance) are compared to animal innate and (or general) resistance and specific immunity are emphasized

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Table 1 Common and distinctive traits of animal and plant immunity (see text for details)
Characteristic Animal innate Plant non-host resistance Animal adaptive immunity Plant host resistance
immunity

Receptors Nonclonal, encoded in Nonclonal, encoded in Clonal, rearranged during development Nonclonal, encoded in
the germline the germline (somatic recombination) the germline
Specificity No No Yes Yes
Self tolerance Yes Yes/no (may induce non- Yes/no (may induce autoimmune yes
host resistance) disorders)
Autoimmunity No ? Yes ?
Memory No No Yes ?

Autoimmunity enemies that are metabolically similar to their own,

such as insects and pathogens, sometimes incurring in
Due to adaptive immunity, animals experienced a autotoxicity. Generally, plants avoid these side
failure of the mechanisms normally responsible for effects by the compartmentalization of chemicals in
maintaining self-tolerance. Autoimmune diseases, cell vacuoles, specialized organelles, nonplasmic or
caused by abnormal immune responses directed extraplasmic compartments, or ad hoc secreting
against self antigens (autoantigens), occur when tissues and organs such as glandular trichomes.
immature self-reactive T and B cells escape the Besides, secondary compounds may occur in plant
clonal deletion, an apoptotic cell death, and lympho- cell as inactive precursors, becoming toxic by some
cyte central tolerance is broken in thymus and bone events during cell disturbance, when the precursors
marrow, respectively. Furthermore, autoimmunity and their hydrolizing enzymes come into contact in
may result from failure of mature T cell tolerance the same compartment [35, 36].
in peripheral tissues, rather than in the generative Notwithstanding, a form of self perception may
lymphoid organs [14]. also occur in plant, with the recognition of altered or
In default of haematopoietic organs and immune wrong self-structural components, such as oligoga-
cells, plants overcome autoimmune disorders. How- lacturonides. These are able to trigger a general non-
ever, if we consider autoimmunity as a general host resistance, rather than an autoimmune disease,
deregulation of immune system, also plant may be although they cannot be strictly considered PAMPs.
exposed to the detrimental effects of their own Oligogalacturonides derive from the degradation of
defence strategies, such as those arising from fitness homogalacturonan (polygalacturonic acid), the main
costs. These are referred to as the trade off between component of plant cell wall pectins, by fungal
resources allocated for growth and reproduction and polygalacturonases (PGs), whereas elicitor-active
disease resistance [7]. In plants, defence mechanisms oligogalacturonides (polymerization degree 8–10)
are highly expensive, from the metabolic point of are produced by the modulation of PGs activity due
view. Due to their sessile habitus, plants are unable to to plant polygalacturonase-inhibiting proteins
avoid the worsening environmental conditions, as (PGIPs) [37].
well as they cannot escape the plethora of the laying
before biotic stresses, thus, unlike animals, evolved
an huge number of different secondary metabolites Conclusions
(i.e. phenilpropanoids, isoprenoids, alkaloids) to
overcome any danger. In this view, a diversion of In vertebrates, the adaptive immunity warrants the
essential available resource, more than required, from specificity of the defence response, due to the ability
growth to defence, may occur in condition of low of generating a vast array of pathogen/antigen
pathogen pressure [7]. Moreover, as a consequence of specific receptors and clonal expansion of antigen
the shift between primary and secondary metabolism, specific effector cells selected by receptor gene
plants are faced with the problem of poisoning rearrangement. On the contrary, innate immunity,

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