We examined the localization of the anti-apoptotic molecule Bcl-2 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis (EAE). Western blot analysis showed that Bcl-2 was constitutively expressed in normal spinal cords, and weakly increased in response to complete Freund's adjuvant(CFA) immunization. In EAE, with infiltration of inflammatory cells into spinal cords, Bcl-2 declined during the peak stage and further decreased during the recovery stage. Immunohistochemically, some neurons and glial cells constitutively expressed Bcl-2 in normal rat spinal cords. In the spinal cords of rats with EAE, Bcl-2 was also immunoreacted in some perivascular inflammatory cells while some brain cells, such as neurons and GFAP (+) astrocytes showed less Bcl-2 immunoreaction.These findings suggest that in EAE, Bcl-2 expression in the CNS host cells decreases with CNS inflammation, possibly progressing to cell death in some cases, while the survival of host cells, including neurons, astrocytes, and some inflammatory cells, is associated with activation of the anti-apoptotic molecule Bcl-2. Taking all into considerations, its is postulated that Bcl-2 either beneficially or detrimentally functions in some host cells depending on the activation stage of each cell type.