VISIONS AND PERSPECTIVES 


ISJ 8: 153-161, 2011                                                                  ISSN 1824-307X 
 
 

VISIONS AND PERSPECTIVES 
 
The ‘immunology trap’ of anthozoans 
 
B Rinkevich 
 
National Institute of Oceanography, Tel Shikmona, P.O. Box 8030, Haifa 31080, Israel 
 
 

   Accepted August 08, 2011 
 

Abstract 
Organisms commonly respond to infectious agents via effector arms of immune systems. 

However, whereas innate immunity in vertebrates has been intensely investigated, we still strive to 
understand how cnidarians’ immunity operates, consulting literature that is rife with unsubstantiated 
statements. Here I contend that the striking superficial similarities with regard to some vertebrate 
genes promote the false notion that considers vertebrate’s and cnidarian’s immunities as homologous. 
This is enhanced by intermingling allorecognition with host-parasite interactions and by synthetic 
comparisons of anthozoans-vertebrates putative immune genes. As complex as it is, cnidarian’s 
historecognition is probably not associated with host-parasite/disease responses and studies on 
anthozoan host-parasite interactions are not yet supported by underlying mechanisms. Therefore, I 
demarcate allorecognition from other aspects of anthozoan immunity and discuss the lack of research 
studies on the anecdotally recorded anthozoan phagocytes. Further attention is given to the roles of 
‘non-immunological defenses’, stand-alone defense mechanisms that respond to environmental 
assaults independently of immunity, also mistakenly regarded as revealing immune properties. 
Because defining immunity in the Anthozoa remains deficient, reflecting the needs for improved 
distinction between historecognition and host-response/disease disciplines, it is required to establish 
an accepted synthesis for what immunity in cnidarians is or is not, and to evaluate changes in 
immunocompetence through quantitative approaches. Following the current state-of-the-art on 
cnidarian immunity, six counsels for re-evaluating immune criteria are offered. 
 
Key Words: allorecognition, Cnidaria, coral, disease, innate immunity, non-immunological defenses 

 

 
Scientia vincere tenebras (conquering darkness 
by science) 

 
The prevalence of diseases in reef organisms, 

many of which are highly virulent (Weil et al., 2006; 
Mydlarz et al., 2010; Reed et al., 2010) has 
stimulated scientific discussion on its causes and 
corals’ immune mediated mechanisms (Mydlarz et 
al., 2006, 2009, 2010; Reed et al., 2010), all based 
on the known abilities of reef organisms to display 
discriminatory tissue reactions to foreign grafts 
(allorecognition; particularly corals; Rinkevich, 2004, 
2011). In addition, corals exhibit a suite of effector 
mechanisms to rid themselves of sediment, settling 
organisms (including pathogens), on top of cellular 
(phagocytic cells; Bigger and Olano, 1993; Olano 
and Bigger, 2000; Mydlarz et al., 2008) and 
biochemical/antimicrobial properties, usually with 
broad spectrum of antimicrobial activities (Jensen, 
___________________________________________________________________________ 

 
Corresponding author:  
Buki Rinkevich 
National Institute of Oceanography, Tel Shikmona 
P.O. Box 8030, Haifa 31080, Israel 
E-mail: buki@ocean.org.il 

 
 
 

1996; Koh, 1997; Kim et al., 2000a, b; Petes et al., 
2003; Ritchie, 2006; Mydlarz and Harvell, 2007; 
Couch et al., 2008; Gochfeld and Aeby, 2008; 
Kvennefors et al., 2008; Palmer et al., 2008; Dunn, 
2009; Mydlarz et al., 2009). Recent studies have 
also scanned anthozoans genomes to elucidate 
immune pathways and immune gene families (Miller 
et al., 2007; Anderson and Gilchrist, 2008; Hayes et 
al., 2010; Oren et al., 2010; Polato et al., 2010). I 
contend that these studies, cumulatively, have led to 
the vague impression that we know what immunity 
in the Anthozoa is. 

This is not the situation. Whilst the vertebrate 
innate immunity has been the subject of intense 
investigation, revealing to a great extent an 
overwhelming complex system (e.g., Du Pasquier, 
2005; Ellis et al., 2011), the research on anthozoan 
immunology suffers from documentation paucity and 
a lack of an accepted synthesis of what innate 
immunity is or is not (Loker et al., 2004; Rinkevich, 
2011). Also, the synthetic comparisons of cnidarians 
genes with seemingly counterpart vertebrate 

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immune genes carried very limited valid information 
on the nature of anthozoan immunity. I further claim 
that the frequent use of buzz words (e.g., 
immunological ‘tool kit’; Miller et al., 2007) and the 
tendency to mix allorecognition with host-parasite 
interactions (e.g., Mydlarz et al., 2006) have been 
erroneously practiced as delivering evidence for 
cnidarian innate immunity, or have been 
inappropriately applied to describe immunological 
responses of reef corals, such as to climate change 
deliverables (e.g., Mydlarz et al., 2009, 2010; Reed 
et al., 2010). Here, I further contend that addressing 
anthozoan immunity by means of deduced genomic 
sequences or gene homology comparisons amidst 
vague descriptions of the underlying mechanisms 
(without having a basic knowledge on the nature of 
anthozoan immunity) is an inadequate approach, 
leading to invalid conclusions and rendering this 
discipline imprecise and elusive. This essay 
accentuates the fact that we still strive to 
understand what immunity in the Cnidaria is and 
how cnidarian immunity operates, and that until 
these are achieved any untenable conclusion could 
lead to erroneous assumptions.  

 
Cnidarian immunity- historecognition 

 
Anthozoans are sessile organisms that cannot 

move away from points of settlement (or exhibit very 
restricted movement capabilities), sometimes living 
in densely populated communities, in environments 
that are laden with infectious agents. Dense 
populations also lead to allogeneic and xenogeneic 
encounters with other permanently attached-to-
hard-surfaces organisms, which settle in close 
proximity. The literature attests that anthozoans (as 
all cnidarians) do not harbor specialized immune 
cells, wandering discriminatory cells or circulatory 
systems. However, they exhibit surprisingly complex 
sets of allorecognition and xenorecognition 
phenomena, exemplified by extreme allotypic 
diversity, wide range of effector arms, un-
confounded immunological specificity, quasi-
immunological memory, allogeneic maturation, 
fusion events that lead to chimerism, and episodes 
associated with ‘ecological immunity’, e.g., 
intraspecific and interspecific competitions (reviewed 
in Lang and Chornesky, 1990; Leddy and Green, 
1991; Rinkevich 1996a, b, 1999, 2004, 2011). 

The effector mechanisms that are used by the 
anthozoans during allogeneic/xenogeneic 
challenges are enormously complex. The list 
includes contact avoidance through chemical 
sensing, allelopathy, barrier formation, tissue and 
skeletal overgrowths, development of sweeper 
tentacles, employment of mesenterial filaments, 
creation of pseudofusions, morphological resorption 
of chimeric individuals, bleaching, retarded growth 
rates, transitory fusions, nematocyst firing, 
developing of delayed responses, necrosis 
formation, tissue growth without calcification, 
attraction of motile phagocytic cells, retreat growths, 
allogeneic reversals and more (details and reviews 
in Hildemann et al., 1979; Bak et al., 1982; 
Rinkevich and Loya, 1983; Hidaka, 1985; Sauer et 
al., 1986; Rinkevich and Weissman, 1987; 
Chornesky, 1989; Lang and Chornesky, 1990; 

Romano, 1990; Leddy and Green, 1991; Salter-Cid 
and Bigger, 1991; Alino et al., 1992; Rinkevich et 
al., 1993, 1994; Tanner, 1993, 1997; Chadwick-
Furman and Rinkevich, 1994; Ding et al., 1994; 
Frank and Rinkevich, 1994, 2001; Jokiel and Bigger, 
1994; Frank et al., 1995, 1996, 1997; Bruno and 
Witman, 1996; Rinkevich 1996a, 2004, 2011; Van 
Veghel et al., 1996; Griffith, 1997; Hidaka et al., 
1997; Abelson and Loya, 1999; Peach and Hoegh-
Guldberg, 1999; Aerts, 2000; Olano and Bigger, 
2000; Rinkevich and Sakai, 2001; Barki et al., 2002; 
Lapid et al., 2004; Nozawa and Loya, 2005; Lapid 
and Chadwick, 2006; Amar and Rinkevich, 2008, 
2010). 

However, many of the phenomenological 
outcomes of cnidarian historecognition offer little in 
terms of the cellular and molecular constituents that 
lead to the morphological outcomes. As complex as 
they are, these historecognition attributes for 
rejecting alien tissues are probably not associated 
with host-parasitic and disease responses in the 
cnidarians (Rinkevich, 2011). Moreover, based on 
our current knowledge, most discussions on 
anthozoan host parasitic interactions (see below) 
are weak and flawed because they are not yet 
supported by any elucidated underlying mechanism. 

 
Cnidarian immunity- phagocytosis and 
associates 

 
As I specified above, the scientific propensity 

that combines cnidarian historecognition 
phenomena with host-parasitic/disease events has 
emerged as a serious obstacle in elucidating the 
nature of cnidarian (mainly reef corals) immunology 
(Rinkevich, 2011) and its cellular components. 
Therefore, it is not surprising to find in the literature 
discussions, merging the concept of invertebrates’ 
immunity with vague, generalized immunological 
phrases (like ‘the invertebrate immune system is 
based on self/nonself recognition and cellular and 
humoral processes’ [Mydlarz et al., 2006]), or 
immunological properties, under a unified 
‘immunological umbrella’. 

One such example for ill-chosen practice in the 
research of anthozoan immunity is the phenomenon 
of phagocytosis and its associated molecular 
cascades. Indeed, the predominant mechanism of 
innate immunity in excluding parasitic/infectious 
forms involves phagocytosis by immune cells. 
However, the literature on anthozoan immunity, 
while documenting a wide repertoire of allogeneic 
phenomena (Hildemann et al., 1977,1979; Leddy 
and Green, 1991; Rinkevich 1996a, 2004, 2011), 
does not detail any clearly mounted defensive 
response on the cellular level, not any evidence for 
phagocytosis response, nor any cell type that 
specifically disables infectious agents, or targets 
direct elimination of infected cells. This argument is 
further illuminated by a recent study on Acropora 
pathogenesis (Work and Aeby, 2011) that has 
employed histological observations on coral lesions. 
Indeed, very few studies (neither one was 
performed on hermatypic corals) have documented 
the participation of motile phagocytic cells, epithelial 
cells, and amebocytes (no specialized phagocytic 
cells) in cnidarian’s biological phenomena, mostly in 

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wound healing scenarios (Mezaros and Bigger, 
1999; Olano and Bigger, 2000), but also in response 
to general stressors (Mydlarz et al., 2008). In a more 
detailed study on a sea anemone (Hutton and 
Smith, 1996), phagocytosis by amebocytes was 
found to be inefficient, as only about 40 % of the 
cells were observed to ingest bacteria in vitro in 
over 45 min. These amebocytes, however, showed 
some antibacterial properties, primarily, when cells 
were lyzed (Hutton and Smith, 1996). 

In association with phagocytosis, cnidarians 
also possess some hemolytic polypeptids in 
celentric fluids (Meinardi et al., 1994), peroxidase 
activities (Mydlarz and Harvell, 2007), antifungal 
and antibacterial lipid metabolites (Koh, 1997; Kim 
et al., 2000a; Dunn, 2009), members of the 
complement system (Dishaw et al., 2005; Miller et 
al., 2007; Dunn, 2009; Kimura et al., 2009), and 
lectins (Kvennefors et al., 2008) which, again, 
without any direct verification, are conjectured to be 
involved in the animals’ immune reactions to 
pathogenic and parasitic insults. This specifically 
applies to the documentation on phenoloxidase-
activating pathways in Anthozoa (Petes et al., 2003; 
Mydlarz and Harvell, 2007; Palmer et al., 2008). 
While activating this melanin synthesis cascade is 
widely documented in invertebrates immunity, it has 
not been confirmed yet whether the anthozoans 
pathway resides in the cellular free compartments 
(e.g., celentric fluids), within either type of 
specialized phagocytes or in any other enigmatic 
cellular compartment (e.g., ‘granular epidermal 
cells’; Palmer et al., 2008) and if it is an effector arm 
of the anthozoan immune defense or just a common 
response to localized or general environmental 
stress, used as a barrier forming device (Petes et 
al., 2003; Mydlarz et al., 2009). 

To my knowledge, there is no detailed research 
study on anthozoan phagocytosis pathways (or 
associated molecular cascades) and no attempt has 
been launched to identify specific disease-borne 
responses on the cellular level. Furthermore, 
nothing is known on how cnidarians’ phagocytes 
recognize a pathogen (e.g., via the use of lectins; 
Pipe, 1990). Amebocytes (but not phagocytosis) 
were anecdotally recorded in diseased anthozoan 
tissues (e.g., Ellner et al., 2007) but more 
information, such as systemic increase in their 
numbers (Mydlarz et al., 2008), apparent cell 
infiltration or cellular proliferation, are needed to 
address the current, immunologically critical 
questions. On the other hand, other possible cellular 
and humoral immune functions may go unnoticed if 
phagocytosis continues to be targeted as the major 
valuable end point for innate immunity. The issue of 
the effector cells (including the alleged roles of 
phagocytes) and associated molecular cascades in 
cnidarian immunity, therefore, remain untested and 
offer no resolution in elucidating disease and host-
parasitic interactions.  

 
Immunity, environmental stressors and global 
changes 

 
Another mistaken research approach tries to 

use selected components of invertebrates’ immune 
systems as the proxy for overall 

immunocompetence; thus an a-priory set of immune 
dysfunction factors and associated conclusions 
become entirely reliant on the immunocompetence 
proxy parameters, leading to erroneous conclusions 
(Ellis et al., 2011). This flawed approach has also 
been expressed in studies on cnidarian immunity, 
such as the attempt to link anthozoans immunity 
with global change impacts (Mydlarz et al., 2009, 
2010), without addressing any actual or quantitative 
change in the overall immunity as a response to 
pathogenic or environmental challenges. 
Unsustainable statements, like those claiming that 
acroporid and pocilloporid corals are more 
susceptible to diseases ‘due to low investment in 
immunity’, or the use of jargon like ‘overall 
immunocompetence’ (Mydlarz et al., 2010) ‘spatial 
immunodynamics’ (Ellner et al., 2007) and ‘factors 
that shape the immune physiology of colonies’ 
(Couch et al., 2008) further convey the wrong 
impression that we are well acquainted with 
cnidarian and coral immunity. This is not the case. 
Some authors (e.g., Lesser et al., 2007) have also 
suggested that with rare exceptions, coral diseases 
should be considered as opportunistic infections 
(syndromes), secondary to exposure to 
physiological insults such as elevated temperature 
that result in uncontrolled growth of bacteria 
normally benign and non-pathogenic. Therefore, 
cnidarians’ disease prevalence may be or may not 
be plausibly associated with global change impacts. 
Hence, any argument on the cnidarians’ tight 
connection between immunity and environmental 
stress necessitates a solid validation, quantification 
and optimization, as generalized for other cases 
(Viney et al., 2005). 

Various studies in other organisms have 
elucidated the interactions and impacts of non-
immunological ‘defenses’ (see below) on 
environmental insults, host parasitic interactions and 
disease prevalence. Relevant examples for non-
immunological ‘defenses’ are impacts of ingested 
plant material on the resistance of insects to their 
parasitic forms (Cory and Hoover, 2006) and the 
possibility that, at least, part of the worldwide 
recorded shell disease syndrome in crustaceans is 
not the resultant of causative agents but a disruptive 
chitin recycling (Vogan et al., 2008). The same may 
apply to documented responses of corals to 
elevated water temperature, such as the enhanced 
expression of heat shock proteins, or the elevation 
in intracellular calcium (Fang et al., 1997). 
Therefore, with regard to coral diseases and 
syndromes (the later probably best characterizes 
coral diseases, as in the vast majority of cases, no 
single causative agent has been found as 
associated with prevalent phenomena), the data 
supporting the connections between cnidarian 
immunity and global change impacts is awkward, 
based largely on anecdotal observations that had 
been generalized to predict anthozoan immunity. It 
hampers our ability to evaluate the genuine impacts 
of environmental stressors and global changes on 
anthozoans immunocompetence. In the same way, 
the possible roles of the yet enigmatic cnidarian 
immunity in the animals’ resistance/susceptibility to 
infectious agents following, for example, bleaching 
events have yet to be explained. 

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The sensitiveness of cnidarians’ immune 
system components to environmental perturbation is 
another unsolved enigma. This issue was 
extensively studied in some marine invertebrates, 
revealing, as an example, that changes in 
phagocytic activity can serve as sensitive parameter 
to environmental insult and to anthropogenically-
induced stressors (Ellis et al., 2011). The cnidarian 
arena remains, however, deficient in spite of 
documentation revealing seasonal and site 
variations, across a geographic region, in disease 
prevalence, antimicrobial and enzyme properties 
(e.g., Ritchie, 2006; Toledo-Hernández et al., 2007; 
Couch et al., 2008). In the same way, very little has 
been comprehended on the crux of the apparent 
coral bleaching in relation to immunity. One ‘non 
immunological’ possibility (see also below) is that 
‘corals that have undergone bleaching become 
more vulnerable to pathogens because the 
protective contributions of their zooxanthellae have 
been lost’ (Loker et al., 2004). In Drosophila, abiotic 
conditions (such as elevated temperature) directly 
affect susceptibility to parasites regardless of the 
functionality of its immune systems (Linder et al., 
2008), a phenomenon that may well be comparable 
to the cnidarians’ increased disease prevalence 
following elevated seawater temperatures. Similarly, 
the variations in resistance of pea aphids attacked 
by parasitoid wasps are related to the impacts of the 
facultative bacterial symbionts, not the host 
genotype’s immunity (Oliver et al., 2005). Stress-
induced diseases in corals also recall the 
phenomenon of the environmentally inflicted stress-
induced senescence, a premature senescence 
induced by various stressors in the absence of 
telomere loss or dysfunction (reviewed in Kuilman et 
al., 2011). 

Understanding how the cnidarian immune 
system responds to environmental challenges and 
how it reflects seasonal variability (e.g., Duchemin 
et al., 2007) are of primary importance. However, 
dealing with global change impacts on immunity 
(without validating what is cnidarian immunity or 
what are the cnidarian immune characteristics), and 
overlooking the roles of environmental, non-
immunological factors in corals’ susceptibility to 
diseases, may lead to wrong conclusions. 
 
Non-immunological ‘defenses’ and how should 
anthozoan immunity be defined? 

 
While organisms do respond to infectious 

agents via the effector arms of their immune 
systems, recent studies have revealed the 
importance of ‘non-immunological defenses’, stand-
alone defense mechanisms that operate 
autonomous to immune system machineries (but 
interact with immune systems) and contribute to the 
organism ability to withstand the impacts of 
infectious agents (reviewed in Parker et al., 2011). 
Examples of non-immunological defenses include 
behavior (e.g., the hygienic behavior in honey bees 
that limits diseases and individual host 
susceptibility; Wilson-Rich et al., 2009), fecundity 
compensation (Petes et al., 2003), physiological 
properties, anorexia, symbiont mediating immunity, 
and social immune mechanisms (Parker et al., 

2011). Some further illustrations for very effective 
non-immunological defenses are (1) the contribution 
of feeding regimen among Daphnia clones to the 
variation recorded in the animals’ susceptibility to 
fungi (Hall et al., 2010), and (2) the secretion of a 
special thick mucus layer, normally expressed in 
non intestinal mucosa, in the intestine of mammals 
resistant to parasite infection, lowering the viability 
of gut-dwelling nematode worms (Hasnain et al., 
2011). 

Likewise, cnidarian ‘chemical warfare’ against 
microbes (Koh, 1997), cytotoxicity of the secreted 
mucus (Ding et al., 1994), the expression of 
chitinolytic enzymes (Douglas et al., 2007), and the 
emancipating of non-specific antifungal and 
antimicrobial compounds (Jensen, 1996; Kim et al., 
2000a, b; Ritchie, 2006; Gochfeld and Aeby, 2008) 
should all be considered as responses associated 
with non-immunological defenses (Lesser et al., 
2007; Parker et al., 2011), unless proven otherwise 
(being an integral participant of immunity, part of the 
effector arm). This could also apply to the vast 
majority of melanization phenomena, as recorded in 
the cnidarians (Petes et al., 2003; Mydlarz and 
Harvell, 2007; Palmer et al., 2008). The arguments 
presented here stand for all cnidarians, including 
hydrozoans, but for clarity and the lack of space this 
assay concentrates on the Anthozoa. 

Here I wish to highlight, again, the claim that 
anthozoan immunity, including recognition elements 
and effector arms, is poorly understood and that the 
term ‘anthozoan immunity’ (and associated 
versions) is wrongly used in a broad sense, ignoring 
the fact that the effector arms used by one group of 
organisms (e.g., vertebrates) are probably different 
from their parallel in other taxa (e.g., corals; Loker et 
al., 2004). Special consideration should be given to 
the demonstrated wide range of interspecific and 
intraspecific differences in responses to any single 
biological/environmental assault, even to different 
levels of a single stressor, or to stressors generated 
by a single cause or in a combination of several 
sources (Ellis et al., 2011). 

Indeed, progress has recently been made in 
expounding the molecular details of cnidarians 
genomes, revealing, by the use of bioinformatics, 
homologous sequences to the vertebrate immune 
genes (Miller et al., 2007; Anderson and Gilchrist, 
2008; Hayes et al., 2010; Oren et al., 2010; Polato 
et al., 2010). However, the striking superficial 
similarities offered with regard to some genes and 
processes in the cnidarians in general and 
anthozoan in particular, are based on the wrong 
notion that considers vertebrate immunity and 
cnidarian immunity as homologous (stemming from 
the rationale that the early appearance of host 
defense indicates that same immune constituents 
are shared by most multicellular organisms; a sort of 
anthropocentrism). 

  
Conclusions- in rerum natura (in the nature of 
things) 

 
Cnidarians, as many other invertebrates 

(Rinkevich, 1999), may employ alternative means to 
generate immunity, making this discipline highly 
complex. In a similar fashion, it has been 

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questioned whether the roles of Toll (a family of 
proteins that triggers innate immunity) in Drosophila 
host resistance are comparable to the roles of Toll-
like receptors in mammalian immunity (Trinchieri 
and Sher, 2007). On the other hand, bioinformatics 
approaches and genome screenings, without 
‘forcing’ vertebrate immunological notions onto 
cnidarian immunity, can be used as powerful tools in 
the research. As immune function in vertebrates is 
one of the biological attributes enriched with genes 
under positive or balancing selection (e.g., 
Fumagalli et al., 2009; Barreiro and Quintana-Murci, 
2010), the two evolutionary forces underlying 
adaptation, employing bioinformatics approaches on 
proposed cnidarians ‘host-pathogen interaction 
genes’ that reveal signatures of adaptation, may 
emerged as the ultimate tool in the research. This is 
further highlighted by the vertebrate/invertebrate 
outcomes that innate immunity systems act in a 
semi-specific way by recognizing pathogen-
associated molecular patterns (PAMPs), which are 
essential and conserved components of pathogen 
entities. 

Although the literature on cnidarian immunity is 
rife with unsubstantiated statements and 
conclusions, it is deficient with regard to what is 
immunity in this group of primitive organisms 
(Rinkevich, 2011). More challenging is the outcome 
that at least some invertebrates possess functional 
equivalents of the acquired responses of 
vertebrates (reviewed in Kvell et al., 2007). While 
this adds to the foreseen complexity of cnidarian 
immunity, as specified above, except for the 
phenomenon of allorecognition where much 
research has been done (Hildemann et al., 1979; 
Leddy and Green, 1991; Rinkevich 1996a, 2004, 
2011), we are still limited in our understanding of 
what is cnidarian immunity in general, and do not 
fundamentally grasp yet coral immunity, in 
particular. Recent approaches and research 
attempts that have delved into the molecular level 
(trying to infer analogous from the vertebrate arena, 
before exploring the full repertoire of the 
invertebrates morphological and cellular 
mechanisms) run the risk of overlooking the real 
phenomenological outcomes, and neglect the 
possible new immunity avenues explored by the 
Cnidaria (Little et al., 2005) by falling into the 
‘homology trap’ (Klein, 1997). It is also dangerous to 
tightly connect other phenomena, like those 
associating coral tumors (Domart-Coulonet al., 
2006) with coral immunity (Palmer et al., 2008; 
Mydlarz et al., 2010). The only real 
phenomenological homology between marine 
invertebrates and vertebrate immunities is probably 
allorecognition, marked by the explicit notion that 
the mechanisms underlying them are similar only in 
the general paradigm of self/nonself recognition 
(Rinkevich, 2011). The effector arms and expression 
pathways, all evolving in harmony for orchestrating 
the immunocompetence in allorecognition and 
infections/disease responses, are probably 
disparate, thus conclusions for the nature of each 
component of innate immunity can be reached only 
through controlled experiments. Clearly, the 
incomplete understanding of anthozoan 

immunocompetence hampers our ability to study 
immune related responses. 

Immunity in invertebrates was for long analyzed 
in terms of the overall response, resulting in 
misunderstandings concerning its biological 
properties (Brehélin

 
and Roch, 2008). To overcome 

such a difficulty, Hildemann et al. (1977, 1979) have 
proposed a minimal set of criteria to test 
invertebrates’ immunity, a major step in the research 
since it put forth, for the first time, a defined set of 
criteria required for use of a term. This led to 
discussions and rebuttals for validity, exclusion or 
inclusion of immunological criteria in experimental 
outcomes, or what is required to meet those criteria. 
However, even after more than three decades of 
research on coral biology, very little is known about 
coral immunology, even though much work exists 
on historecognition reactions. In this regards, 
researchers have attempted to provide some 
empirical evidence of what that immune system may 
possess (i.e., gene products) as well as some 
preliminary, even anecdotal, evidence as to how 
that system may function (e.g., phagocytosis), all 
without much success to reveal the nature of 
cnidarian immunity. I argue that the extent to which 
anthozoan ‘immunity’ (but not historecognition) is 
modulated or modified by parasitic forms, 
environmentally laden microbes, or environmental 
insults cannot be inferred from the current literature. 
Therefore reconsidering the approach for ‘criteria’ 
(Hildemann et al., 1977, 1979) in the research of 
cnidarian immunity/diseases/host-parasitic 
interactions may clear up the way for understanding 
the impacts of environmental insults on anthozoan 
immunocompetence. 

The current state-of-the-art reveals that we still 
do not really know what immunity in the Cnidaria is. 
Hence, before statements on cnidarian immunity 
can be made (like the roles of immunocompetence 
in coral diseases, impacts of environmental stress 
on coral immunity), we need an improved distinction 
between historecognition, host-response and 
disease disciplines in the Cnidaria. Then, the 
research on anthozoans immunity needs (a) to 
establish, with high standards of scientific scrutiny, 
an accepted synthesis of what immunity in this 
group of organisms is or is not (e.g., theoretically, as 
long as pathogens are correctly identified, there is 
no need for the fine detection of all non-self versus 
self), (b) to recognize that the ability of corals to 
ward off opportunistic infections and the capacity for 
highly regulated allorecognition might have evolved 
from different origins under differing evolutionary 
pressures. Unless proven otherwise, both 
phenomena should be considered independently, 
thus any scientific outcome to be assigned to either 
immunity route, not a-priori shared by both, (c) to 
evaluate the changes in immunocompetence 
following virulent/environmental assaults through 
quantitative approaches, such as the ‘clearance 
efficiency’ assay, phagocytic index, cellular reactive 
oxygen intermediate production, bactericidal activity 
of cells and other assays (Ellis et al., 2011), (d) to 
perform ‘’experimental immunization assays’, for 
elucidating the properties of cnidarians immunity. 
Such an approach may test the likelihood that 

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infection can impose changes in the activity of 
certain highly defined immune functions (e.g., 
nonspecific immunological priming). For example, 
Moret and Siva-Jothy (2003) showed that injection 
of bacterial cell wall components increased the 
resistance of insects against a fungus, up regulating 
of a generic immune response, also showing that an 
induced response can occur without specificity, (e) 
to clarify the roles and importance of ‘non-
immunological defenses’ (like mucus shedding in 
corals) in cnidarian immunosurveillance, and (f) to 
employ bioinformatics approaches and genome 
screenings not only as comparative tools. Molecular 
biology approaches should be exercised to better 
design functional experiments of cnidarian host-
pathogen interactions and immunosurveillance (as 
successfully employed on cnidarian 
historecognition) and to analyze the footprint of 
adaptive selection signatures in the innate immune 
mechanisms. Since the ‘immunology trap’ is not 
unique to the Cnidaria, above six major suggestions 
for re-evaluating immune criteria may also be 
utilized in the research of other invertebrate taxa. 
 
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