Immunogenetics

, Volume 21, Issue 1, pp 33–38

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

  • Premkumar Christadoss
  • Jon M. Lindstrom
  • Roger W. Melvold
  • Norman Talal
Article

DOI: 10.1007/BF00372239

Cite this article as:
Christadoss, P., Lindstrom, J.M., Melvold, R.W. et al. Immunogenetics (1985) 21: 33. doi:10.1007/BF00372239

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.

Abbreviations used in this paper

MG

myasthenia gravis

AChR

acetylcholine receptors

EAMG

experimental autoimmune myasthenia gravis

Ir

immune response

B6

C57BL/6J

bm12

B6.C-H-2bm12

CFA

complete Freund's adjuvant

LNC

lymph node cells

PPD

purified protein derivative

Copyright information

© Springer-Verlag 1985

Authors and Affiliations

  • Premkumar Christadoss
    • 1
  • Jon M. Lindstrom
    • 2
  • Roger W. Melvold
    • 3
  • Norman Talal
    • 1
  1. 1.The Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, and Department of MedicineThe University of Texas Health Science Center at San AntonioSan Antonio
  2. 2.The Receptor Biology LabThe Salk InstituteLa Jolla
  3. 3.The Medical Oncology SectionNorth Western UniversityChicago
  4. 4.Department of Medicine, Division of Clinical ImmunologyThe University of Texas Health Science CenterSan Antonio

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