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

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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.

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Abbreviations

MG:

myasthenia gravis

AChR:

acetylcholine receptors

EAMG:

experimental autoimmune myasthenia gravis

Ir:

immune response

B6:

C57BL/6J

bm12 :

B6.C-H-2 bm12

CFA:

complete Freund's adjuvant

LNC:

lymph node cells

PPD:

purified protein derivative

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

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  • DOI: https://doi.org/10.1007/BF00372239

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