Abstract
T-cell apoptosis in the CNS is an effective mechanism for the noninflammatory resolution of autoimmune T-cell infiltrates. Ingestion of apoptotic leukocytes by microglia results in an efficient clearance of the inflammatory infiltrate, followed by a profound downregulation of proinflammatory phagocyte immune functions. The effects of different immunomodulatory agents on Lewis rat microglial phagocytosis of apoptotic autologous thymocytes or myelin-basic protein (MBP)-specific, encephalitogenic T-cells were investigated using a standardized, light microscopical in vitro phagocytosis assay. Pretreatment of microglia with polyclonal 7S immunoglobulins (IVIg) decreased the phagocytosis of apoptotic thymocytes by 38.2% ( p<0.0001). Also, immunoglobulin F(ab′) 2 fragments decreased microglial phagocytosis, suggesting an Fc receptor-independent mechanism. Similar results were obtained using MBP-specific T-cells. Pretreatment of microglia with IFN-γ increased the phagocytosis of apoptotic cells by 65.4%, which was to a large extent counteracted by IVIg. Glatiramer acetate (GLAT) did not exert an effect on microglial phagocytosis, while methylprednisolone (MP) induced microglial apoptosis in vitro. These results indicate that IVIg has a high potential to inhibit microglial phagocytosis of apoptotic inflammatory T-cells even under proinflammatory conditions and extend our view of the complex immunomodulatory effects of IVIg.
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