Mice bearing the H-2bhaplotype are susceptible to the development of experimental autoimmune myasthenia gravis (EAMG), induced by acetylcholine receptor (AChR) autoimmunity. One of the genes influencing EAMG susceptibility has been mapped to the Ablocus of the major histocompatibility complex, and the Aβ chain has been implicated in the pathogenesis. Mice of the H-2bhaplotype, including C57BL/10 (B10), have a genomic deletion of the Eαgene and therefore fail to express the E molecule on their cell surface. To test the hypothesis that failure to express the cell surface E molecule in B10 mice contributes to EAMG pathogenesis, Einfαsup ktransgenic B10 mice expressing the T molecule were examined. Expression of the E molecule in Einfαsup ktransgenic B10 mice partially prevented the development of EAMG.
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