The role of immuno-recognition in defense mechanisms of decapod crustaceans has been a subject of speculation since the initial studies on phagocytosis in daphnids were conducted by Metchnikoff at the beginning of the twentieth century. Immuno-recognition is inherent to phenomena which allow the animal to distinguish self from non self and provides the foundation for classical vertebrate serologic mechanisms. Both cellular and humoral components are involved.

Although all invertebrates examined so far have been shown to possess serologic mechanisms which resemble those observed in higher vertebrates, many classical immunologists tend to distinguish invertebrate serologic responses from vertebrate serologic responses on the basis of: 1) the absence of immunoglobulin, 2) purported absence of "memory" and inducibility- and 3) the lack of specificity associated with invertebrate serologic responses.

Since invertebrates do not synthesize immunoglobulins, other types of molecules must be involved in the recognition of non self components. Lectins which are ubiquitous among invertebrates and are known to be present in most tissues and body fluids (Gold, E. R. and P. Balding. Plant and Animal Lectins. Excerpta Medica, Amsterdam, 1975; Cohen, E. and G. R. Vasta, In: Developmental Immunology. Clinical Problems and Aging (E. L. Cooper and M. A. B. Brazier, Eds.), pp 99-108. Academic Press, New York, 1982) are likely candidates for the role of recognition molecules in penaeids.

Cellular mechanisms, primarily phagocytosis, are generally believed to be the principal mechanisms involved in internal defense mechanisms of decapod crustaceans and other invertebrates. In higher vertebrates, phagocytosis is stimulated by the presence of specific immunoglobulin molecules on antigenic surfaces and activation of C3b complement. However, it is well known that phagocytosis also occurs in those animals in the absence of serum antibodies. Such "non immunologic" or "non specific" phagocytic processes have been observed with bacteria and various other types of biological as well as non biological particles. Some investigators have speculated that net surface charge or hydrophobicity of a particle determined whether it would be recognized by phagocytic cells during "non immunologic" phagocytic processes but substantiating experimental evidence is lacking (Griffin, F. M. In: Advances in Host Defense Mechanisms (J. I. Galtin and A. Fauci, eds) Vol 1: 31 -55, Raven Press, New York). Based upon evidence from several laboratories including our own, we believe that carbohydrate-lectin interactions provide the basis for immuno-recognition in shrimp and that such interactions are conserved throughout the biological kingdom in "non-immunologic" phagocytic processes. Such interactions occur in three ways (summarized in the attached figure): 1) between sugars on the surface of the phagocytes and lectins on the surface of other cells; 2) between lectins on the surface of the phagocytes and sugars on other cells and 3) by extracellular lectins that form bridges between sugars on both types of cell (Sharon, N. Immunology Today 5, 143, 1984).

Figure. Schematic representation of lectin mediated interactions of hemocytes with bacterial cells.

Hemocyte CHO moieties bind lectins and cells. Typical of most cells, hemocytes possess a sugar moiety which consists of the oligosaccharide units of membrane glycoproteins and glycolipids. Information concerning cell surface sugars is primarily based upon experiments with plant lectins. Lectins bind to such sugar receptors and the binding is inhibited or reversed by the sugars for which the lectins are specific. Binding of lectins to sugars on certain cells, e.g. macrophages, frequently induce physiologic changes (eg mitosis) in the cell.

Since lectins are multivalent, they could form bridges between hemocytes and other types of cell. Experimental studies are underway which will test this relationship in penaeids. Carbohydrate specific binding of Con A to the surface of mouse macrophages mediate attachment but not phagocytosis of Bacillus subtilis (Allen et al, Exp. Cell Res. 68, 466, 1970).

Surface lectins confer susceptibility of bacterial cells to phagocytosis. It is well known that adherence of many gram-negative bacteria to animal cells is specifically inhibited by mannose and methyl alpha mannoside (Duguid, J. P and D. C. Old In: Bacterial Adherence (E. H. Beac hey, ed) pp. 186 Chapman and Hall, London). This adherence is probably an essential step in the pathogenesis of infectious diseases. In the case of Escherichia coli, the common form of the mannose-specific lectins are type-l-fimbriae (or pili). These bacteria bind avidly through their surface lectins and binding elicits a burst of metabolic activity in the phagocytes, followed by a sequence of events characteristic for the phagocytosis of opsonized bacteria. None of the reactions occur when bacteria and macrophages are mixed in the presence of mannose. (Silverblatt, F. J. et al., Infect. Immun. 24, 218, 1979).

Binding and uptake by macrophage surface lectins. In addition to the presence of various carbohydrate moieties, cell surfaces also possess a variety of lectins. The best characterized of these is the galactose-specific lectin found on liver, spleen and peritoneal macrophages. These macrophages bind and phagocytose erythrocytes that have been treated with sialidase to expose galactose residues on their surfaces.

Conclusion

No doubt lectin-carbohydrate interactions play a key role in defense mechanisms of decapods. Recent studies which validate the protective value of various bacterins in lobsters, shrimp and various decapods indicate that lectins are also inducible and are implicated in memory functions thus fulfilling certain of the criteria for "legitimate" immunologic phenomenon ascribed to vertebrates. Lectin-carbohydrate interactions could provide a host-defense mechanism in higher vertebrates shortly after microbial (viral?) infection and prior to establishment of an immune state, or in tissues where normal opsonic activity is poor.