The autoimmune disease of the central nervous system (CNS), experimental allergic encephalomyelitis (EAE), is induced by challenge of genetically susceptible animals with spinal cord homogenates or myelin basic protein (MBP). Chronic and relapsing forms of the disease have some similarities to human demyelinating disorders, namely, multiple sclerosis, and are of particular interest. EAE can be transferred passively with sensitized lymphoid cells into syngeneic animals but transferred EAE has been believed to have limited relevance to human disease because it is usually monophasic and manifested by minimal demyelination. We report here that a single transfer of MBP-sensitized lymph node cells or T cell, in the absence of a peripheral antigen depot, leads to both acute EAE with significant primary demyelination, and chronic relapsing disease with lesions typical of demyelination over a long period. These findings have major implications for the immunological mechanisms involved in experimental and human demyelinating diseases.