E inf? supk transgene in B10 mice suppresses the development of myasthenia gravis

1 April 1990

journal article
Published by Springer Nature in Immunogenetics

Vol. 31 (4)
https://doi.org/10.1007/bf00204895

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 _infα ^supk transgenic B10 mice expressing the T molecule were examined. Expression of the E molecule in E _infα ^supk transgenic B10 mice partially prevented the development of EAMG.

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