Ek alpha transgene in B10 mice suppresses the development of myasthenia gravis.

Mice bearing the H-2b haplotype 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 Ab locus of the major histocompatibility complex, and the A beta chain has been implicated in the pathogenesis. Mice of the H-2b haplotype, including C57BL/10 (B10), have a genomic deletion of the E alpha gene 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, Ek alpha transgenic B10 mice expressing the E molecule were examined. Expression of the E molecule in Ek alpha transgenic B10 mice partially prevented the development of EAMG.