Einfαsup k transgene in B10 mice suppresses the development of myasthenia gravis

Premkumar Christadoss, Chella S. David, Mohan Shenoy, Steve Keve

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)241-244
Number of pages4
JournalImmunogenetics
Volume31
Issue number4
DOIs
StatePublished - Apr 1 1990

ASJC Scopus subject areas

  • Immunology
  • Genetics

Fingerprint Dive into the research topics of 'E<sub>infα</sub><sup>sup k</sup> transgene in B10 mice suppresses the development of myasthenia gravis'. Together they form a unique fingerprint.

  • Cite this