ABSTRACT
Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the II MHC I-Ag7 nervous system (CNS) believed to be autoimmune in origin. MS affects approximately 300,000 people in the United States with a female to male ratio of 2:1. Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease of the CNS inducible II experimental animals by immunization with protein constituents of CNS myelin. EAE is a paralytic disease characterized by the presence of inflammatory infiltrates and demyelination in the CNS. Because of these and other features, EAE has been used as a model of MS. Studies in the EAE model have contributed greatly to our understanding of the mechanisms involved in the pathogenesis of CNS autoimmunity. The EAE model has also been used to evaluate therapeutic approaches for the treatment of MS. This chapter will review the history of the EAE model and its contribution to our understanding of the molecules and genes involved in initiating CNS autoimmunity.
