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

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

doi:10.1007/BF00372239

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

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

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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.

Original language	English (US)
Pages (from-to)	33-38
Number of pages	6
Journal	Immunogenetics
Volume	21
Issue number	1
DOIs	https://doi.org/10.1007/BF00372239
State	Published - Jan 1985
Externally published	Yes

ASJC Scopus subject areas

Immunology
Genetics

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title = "Mutation at I-A beta chain prevents experimental autoimmune myasthenia gravis",

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.",

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AU - Christadoss, Premkumar

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AB - 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.

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

Abstract

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