摘要： Retinitis pigmentosa is a devastating, blinding disorder that affects 1 in 4000 people worldwide. During the progression of the disorder, phagocytic clearance of dead photoreceptor cell bodies has a protective role by preventing additional retinal damage from accumulation of cellular debris. However, the cells responsible for the clearance remain unidentified. Taking advantage of a mouse model of retinitis pigmentosa (RhoP23H/P23H), we clarified the roles of M ¨uller glia in the phagocytosis of rod photoreceptor cells. During the early stage of retinal degeneration, M ¨uller glial cells participated in the phagocytosis of dying or dead rod photoreceptors throughout the outer nuclear layer. Nearly 50% of M ¨uller glia engaged in phagocytosis. Among the M ¨uller phagosomes, >90% matured into phagolysosomes. Those observations indicated that M ¨uller glial cells are the primary contributor to phagocytosis. In contrast, macrophages migrate to the inner part of the outer nuclear layer during photoreceptor degeneration, participating in the phagocytosis of a limited population of dying or dead photoreceptor cells. In healthy retinas of wild-type mice, M ¨uller glial cells phagocytosed cell bodies of dead rod photoreceptors albeit at a lower frequency. Taken together, the phagocytic function of M ¨uller glia is responsible for retinal homeostasis and reorganization under normal and pathologic conditions.