Cellular immune response to acetylcholine receptors in murine experimental autoimmune myasthenia gravis

Inhibition with monoclonal anti-I-A antibodies

Premkumar Christadoss, Jon Lindstrom, Norman Talal

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Gene(s) at the I-A subregion of the murine major histocompatibility complex influence susceptibility to experimental autoimmune myasthenia gravis. C57B1/6 mice immunized with acetylcholine receptors (AChR) in complete Freund's adjuvant demonstrated cellular and humoral immune responses to AChR. They developed muscle weakness characteristic of myasthenia gravis and demonstrated a reduction in the muscle AChR content. The kinetics of AChR-specific lymphocyte proliferation generally correlate with anti-AChR antibody response. AChR-specific lymphocyte proliferation was also observed in C57B1/6 splenocytes after secondary immunization with AChR. The in vitro cellular reactivity to AChR in experimental autoimmune myasthenia gravis (EAMG) mice (C57B1/6) was suppressed by monoclonal anti-I-Ab antibodies directed against private (Ia20) or public (Ia8) specificities, suggesting a critical role for these Ia determinants in the cellular immune response to AChR in murine EAMG.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalCellular Immunology
Volume81
Issue number1
DOIs
StatePublished - Oct 1 1983
Externally publishedYes

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Autoimmune Experimental Myasthenia Gravis
Cholinergic Receptors
Cellular Immunity
Antibodies
Lymphocytes
Secondary Immunization
Freund's Adjuvant
Myasthenia Gravis
Muscle Weakness
Humoral Immunity
Major Histocompatibility Complex
Antibody Formation

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

Cellular immune response to acetylcholine receptors in murine experimental autoimmune myasthenia gravis : Inhibition with monoclonal anti-I-A antibodies. / Christadoss, Premkumar; Lindstrom, Jon; Talal, Norman.

In: Cellular Immunology, Vol. 81, No. 1, 01.10.1983, p. 1-8.

Research output: Contribution to journalArticle

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