BOTH RAT AND MOUSE T CELL RECEPTORS SPECIFIC FOR THE ENCEPHALITOGENIC DETERMINANT OF MYELIN BASIC PROTEIN USE SIMILAR V a AND V ß CHAIN GENES EVEN THOUGH THE MAJOR HISTOCOMPATIBILITY COMPLEX AND ENCEPHALITOGENIC DETERMINANTS BEING RECOGNIZED ARE DIFFERENT

The study of an autoimmune disease model such as experimental allergic encephalomyelitis (EAE)' will hopefully reveal a means to control such disease. EAE is an antigen-specific T cell-mediated disease that is considered to be a model for multiple sclerosis due toits similar pattern ofcentral nervous system (CNS) lesions and demyelination (1, 2) . This disease was first noted in patients whohad developed neurological deficits after inoculation with early rabies vaccine preparations containing residual myelin from in vivo brain culture ofthe virus (3). Oneobvious target for regulation of this T cell-mediated disease would be a TCR idiotype . This would require (a) that the disease-inducing T cells respond to one (or a few) auto-antigenic determinant; and (b) that they use a restricted set of TCR genes to recognize this antigen. That a limited number of antigenic determinants are responsible for EAE has been established in several animal models, including mouse, rat, and guinea pig. In all cases, myelin basic protein (MBP) is the target agent (4-6). Using small peptides it was further shown that, in Lewis rat, all ofthe encephalitogenic activity could be localized to the amino acid 68-88 fragment (MBP 68-88) (5, 7) . Thus, a limited region of a single protein, and presumably, therefore, a single or limited number of antigenic determinants, is responsible for activating EAE-inducing T cells (8). Evidence exists both for and against limited TCR repertoire usage in Lewis rat, EAE-inducing (MBP 68-88-reactive)Tcells . It has been shown that protection from disease could be obtained by prior immunization with either inactivated EAE-inducing