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Administration of exogenous 1,25-(OH) 2 D 3 suppresses EAE progression through Rag-1-dependent lymphocyte-mediated mechanisms that restrict CNS infiltration of auto-reactive T cells and macrophages, promote apoptosis of inflammatory cells, and enhance survival of resident CNS cells, an effect associated with decreased macrophage accumulation within the CNS (Nashold et al., 2001