Abstract

Mononuclear phagocytes have been a focus of attention in the cellular biology of proliferative vitreoretinopathy (PVR) for more than ten years. The pattern of phagocyte participation in periretinal traction membrane formation in PVR depends on the etiology, i.e. trauma, rhegmatogenous retinal detachment, previous therapy, i.e. multiple surgical interventions, and the clinical stage of the disease. We have recently identified microglial cells as a distinct cellular population, in membranes from patients with non-traumatic PVR. Current evidence of mononuclear phagocyte function in PVR suggests a role for resident phagocytes of the vitreous and retina in PVR subsequent to rhegmatogenous detachment, and a role for blood-derived monocytes in post-traumatic PVR. The cellular biology of PVR may be much more heterogeneous than previously assumed.

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