Abstract
Phagocytosis is the process whereby cells engulf large particles, usually over 0.5 micro m in diameter. Phagocytosis is triggered by the interaction of opsonins that cover the particle to be internalized with specific receptors on the surface of the phagocyte. The best-studied phagocytic receptors include the Fc receptors (FcR) that bind to the Fc portion of immunoglobulins. Cross-linking of FcR on the phagocyte initiates a variety of signals, which lead through the reorganization of the actin cytoskeleton, and membrane remodeling, to the formation of the phagosome. From recent data, it is becoming clear that FcR-mediated phagocytosis occurs as a series of steps that are regulated in a nonlinear manner and that signaling for phagocytosis does not terminate when the phagosome is formed. Several lipid molecules localize around the nascent phagosome and function as initiators of important signaling pathways for the late stages of phagolysosome formation. In addition, the use of particular signaling molecules may change for different receptors and may also vary depending on the activation or differentiation state of the cell. This review focuses on this new information and presents a model of our present understanding of the signal transduction events that regulate phagocytosis mediated by FcR.
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