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Experimental allergic encephalomyelitis (EAE) serves as a model for autoimmune diseases mediated by T lymphocytes^1,2. Following sensitization to rat, mouse or guinea pig myelin basic protein (MBP) in complete Freund's adjuvant, inbred mouse strains PL/J (H–2^u, SJL/J (H–2^s) and (PL/J × SJL/J)F₁((PLSJ)F₁) develop EAE^3,4. Whereas sensitization to the N-terminal 37 amino-acid peptide of rat or guinea pig MBP [MBP(1–37)] induces EAE in PL/J mice, immunization to the C-terminal peptide (89–169) leads to EAE in SJL/J mice^4,5. The immune response to MBP in (PLSJ)F₁ mice is not co-dominant; sensitization to the N-terminal peptide induces EAE, while sensitization to the C-terminal peptide does not^3,4. We have generated MBP-specific T-cell clones restricted to class II (Ia) antigens of the major histocompatibility complex (MHC) from PL/J and (PLSJ)F₁ mice following sensitization to rat MBP. Two such I–A …