Journal of neuroimmunology
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Tumor necrosis factor alpha (TNF alpha) and lymphotoxin alpha (LT alpha) induce pleiotropic cellular effects through low-affinity 55 kDa type-1 receptors (TNFR1, CD120a) and high-affinity 75 kDa type-2 receptors (TNFR2, CD120b). Both cytokines have potent biological effects on glial cells and are strongly implicated in the pathology of central nervous system (CNS) demyelinating diseases. However, to date, neither constitutive nor cytokine-induced TNFR expression by glial cells have been definitively characterized. ⋯ TNF alpha increases expression of TNFR1 by oligodendrocytes whereas it increases expression of TNFR2 by microglia. Microglia proliferation data suggest that signals transduced through TNFR2 directly or indirectly inhibit signals transduced through TNFR1. Different patterns of TNFR expression by glia at sites of CNS inflammation may be critical in determining whether TNF has activational, proliferative, or cytotoxic effects on these cells.