Cellular receptors and signal transduction in molluscan hemocytes: connections with the innate immune system of vertebrates.

The involvement of circulating hemocytes as the principal cellular effector mediating molluscan immune responses is well established. They participate in a variety of internal defense-related activities including microbial phagocytosis, multicellular encapsulation, and cell-mediated cytotoxicity reactions that are presumed to be initiated through foreign ligand binding to hemocyte receptors and subsequent transduction of the binding signal through the cell resulting in appropriate (or in some cases, inappropriate) hemocyte responses. At present, however, although functional evidence abounds as to the existence of hemocyte "recognition" receptors, few have been characterized at the molecular level. Similarly, signal transduction systems associated with various receptor-mediated hemocyte functions in molluscs are only beginning to be investigated and understood. This review examines what is currently known about the molluscan hemocyte receptors and the putative signal transduction pathways involved in regulating their cellular behaviors/activities. The cumulative data implies the presence of various hemocyte-associated receptors capable of binding specific carbohydrates, extracellular matrix proteins, growth factors, hormones, and cytokines. Moreover, receptor-ligand interactions appear to involve signaling molecules similar to those already recognized in vertebrate immunocyte signal transduction pathways, such as protein kinases A and C, focal adhesion kinase, Src, Ca(2+) and mitogen-activated protein kinase. Overall, the experimental evidence suggests that molluscan immune responses rely on molecules that share homology with those of vertebrate signaling systems. As more information regarding the molecular nature of hemocyte recognition receptors and their associated signaling molecules is accumulated, a clearer picture of how hemocyte immune responses to invading organisms are regulated will begin to emerge.