E_infα^{sup k} transgene in B10 mice suppresses the development of myasthenia gravis

Mice bearing the H-2^bhaplotype 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 A^blocus of the major histocompatibility complex, and the Aβ chain has been implicated in the pathogenesis. Mice of the H-2^bhaplotype, including C57BL/10 (B10), have a genomic deletion of the E_αgene 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, E_infα^{sup k}transgenic B10 mice expressing the T molecule were examined. Expression of the E molecule in E_infα^{sup k}transgenic B10 mice partially prevented the development of EAMG.