Mutation at I-A beta chain prevents experimental autoimmune myasthenia gravis

Premkumar Christadoss, Jon M. Lindstrom, Roger W. Melvold, Norman Talal

Research output: Contribution to journalArticle

85 Scopus citations

Abstract

Immune response (Ir) gene(s) at the I-A subregion of the mouse H-2 complex influence susceptibility to experimental autoimmune myasthenia gravis (EAMG). To determine the importance of the Ir gene product, the Ia antigens, in EAMG pathogenesis, we studied the degree of EAMG susceptibility of an I-A mutant strain, the B6.C-H-2bm12 (bm12), and its parent B6/Kh. According to the cellular, humoral, biochemical, and clinical manifestations of EAMG, the I-A mutation converted an EAMG susceptible strain (B6/Kh) into a relatively resistant strain (bm12). The relative resistance to EAMG induction in bm12 may be due to the lack of Ia.8 and/or la.39 determinants and/or quantitative expression of la antigens.

Original languageEnglish (US)
Pages (from-to)33-38
Number of pages6
JournalImmunogenetics
Volume21
Issue number1
DOIs
StatePublished - Jan 1 1985

ASJC Scopus subject areas

  • Immunology
  • Genetics

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    Christadoss, P., Lindstrom, J. M., Melvold, R. W., & Talal, N. (1985). Mutation at I-A beta chain prevents experimental autoimmune myasthenia gravis. Immunogenetics, 21(1), 33-38. https://doi.org/10.1007/BF00372239