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, 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 Ia.39 determinants and/or quantitative expression of Ia antigens.
D000818:Animals; D000917:Antibody Formation; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology*; D005802:Genes, MHC Class II; D006183:H-2 Antigens / Q000235:genetics*; D000949:Histocompatibility Antigens Class II / Q000235:genetics*; D007111:Immunity, Cellular; D051379:Mice; D008817:Mice, Mutant Strains / Q000276:immunology; D009157:Myasthenia Gravis / Q000235:genetics / Q000276:immunology*; D011950:Receptors, Cholinergic / Q000276:immunology
D006183:H-2 Antigens; D000949:Histocompatibility Antigens Class II; D011950:Receptors, Cholinergic