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Phagocytosis is a cellular process in which specialized phagocytic cells (e.g., macrophages, neutrophils, dendritic cells, retinal pigment epithelial cells) ingest large extracellular particles (such as microbes, apoptotic bodies, or tissue debris) into phagosomes, which subsequently fuse with lysosomes to degrade the contents. This process is finely regulated by a diverse array of cell-surface receptors, including Fc gamma receptors (FcγRs) that bind antibodies, complement receptors that recognize opsonized targets, pattern-recognition receptors (PRRs), scavenger receptors, and other non-opsonic receptors. Actin cytoskeleton remodeling drives particle engulfment, forming membrane protrusions (pseudopods) that envelop the target and complete internalization. Multiple signals—“eat-me” and “don't-eat-me”—help discriminate targets and modulate phagocytosis, with defective clearance leading to disease states such as cancer, autoimmunity, and neurodegeneration. Phagocytosis can be “promoted” clinically or experimentally by targeting receptors, signaling pathways, or membrane properties affecting phagocytic efficiency, but promotion itself is not a defined molecule or receptor.
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