Mutation at IA beta chain prevents experimental autoimmune myasthenia gravis

P Christadoss, JM Lindstrom, RW Melvold, N Talal - Immunogenetics, 1985 - Springer
P Christadoss, JM Lindstrom, RW Melvold, N Talal
Immunogenetics, 1985Springer
Immune response (Ir) gene (s) at the IA 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 IA mutant strain, the B6. CH-2 bm 12 (bm12), and its
parent B6/Kh. According to the cellular, humoral, biochemical, and clinical manifestations of
EAMG, the IA mutation converted an EAMG susceptible strain (B6/Kh) into a relatively …
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-2 bm12 (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.
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