Experimental allergic encephalomyelitls (EAE) Is an autoimmune disease characterized by inflammation and demyellnation in the central nervous system (CNS). Administration of transforming growth factor-β?(TGF-β) has been shown to inhibit EAE. In this study, the possible role of endogenous TGF-β in the regulation of relapsing EAE produced by the transfer of myelin basic protein-specific T cell lines was assessed. Although TGF-β is not present In the normal CNS, this cytokine was detected by immunohistology In areas of central nervous system inflammation in both acute and chronic disease. The administration of anti-TGF-β at the disease onset led to a worsening of the clinical course of EAE and more extensive pathological lesions. These findings provide direct evidence for a role of endogenous TGF-β In the remissions seen in chronic relapsing EAE.