Phagocytic receptors activate and immune inhibitory receptor SIRPα inhibits phagocytosis through paxillin and cofilin.

摘要: The innate-immune function of phagocytosis apoptotic cells, tissue-debris, pathogens and cancer cells is essential for homeostasis, tissue repair, fighting infection combating malignancy. Phagocytosis carried out in the CNS by resident microglia both PNS recruited macrophages. While proceeds, bystander healthy protect themselves sending a “do not eat me” message to phagocytes as CD47 on their surface ligates immune inhibitory receptor SIRPα then produces signaling which inhibits phagocytosis. This helpful mechanism becomes harmful when tissue-debris unhealthy inhibit own employing same mechanism. However, that has been fully revealed. We focus here how “degenerated-myelin” hinders repair axonal injury neurodegenerative diseases. tested whether regulating cytoskeleton through paxillin cofilin since (a) generates mechanical forces drive (b) control function. Paxillin were transiently activated was activated. In contrast, continuously augmented expression knocked-down SIRPα-shRNA. Further, levels phagocytosis, activation positively correlated with one another. Taken together, these observations suggest novel whereby are targeted activating phagocytic receptors produce promoting inhibiting inactivation cofilin.