Abstract
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 supkinfα transgenic B10 mice expressing the T molecule were examined. Expression of the E molecule in E supkinfα transgenic B10 mice partially prevented the development of EAMG.
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Christadoss, P., David, C.S., Shenoy, M. et al. E supkinfα transgene in B10 mice suppresses the development of myasthenia gravis. Immunogenetics 31, 241–244 (1990). https://doi.org/10.1007/BF00204895
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DOI: https://doi.org/10.1007/BF00204895