MUTATION AT I-A BETA-CHAIN PREVENTS EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS

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, the degree of EAMG susceptibility of an I-A mutant strain, the B6.C-H-2bm12 (bm12), and its parent B6/Kh was studied. 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 Ia.39 determinants and/or quantitative expression of Ia antigens.