Résumé
The Pacific oyster Crassostrea gigas is an important cultured species whose production has suffered from recurrent summer mortality events worldwide over the past two decades. In France, these mortality outbreaks have become devastating for the production of juvenile stages since 2008, and have resulted in great economic losses that currently threaten this activity. Studies on oyster immunity have been performed to better understand its response to pathogens, in particular to bacteria of the Vibrio genus and Herpes viruses, both found in moribund oysters. The immune response of C. gigas relies entirely on the innate immune system, in which hemocytes, the oyster circulating blood cells, are the main cellular mediators of the defense system. Activated when pathogen-associated molecular patterns are recognized by plasma soluble or cell surface pattern recognition receptors, hemocytes operate in a coordinated manner with soluble factors in the hemolymph to circumvent the infection. Over the past years, research efforts have substantially increased the knowledge of the molecular bases of oyster immunity, from non-self recognition proteins, to cytokines, signaling pathways and defense effectors including protease inhibitors, hydrolytic enzymes and antimicrobial peptides/proteins. This review describes the present state of our knowledge on the cellular and molecular effectors of oyster immunity, and describes the oyster responses to pathogenic Vibrio and Herpes species.