Influence of T cell specificity on the heterogeneity and disease-causing capability of antibody against the acetylcholine receptor

Trai Ming Yeh, Keith A Krolick

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Adoptive secondary anti-acetylcholine receptor (AChR) antibody responses were examined in rats to evaluate the influence of helper T cell specificity on the nature and disease-causing potential of antibody produced. Mixtures of B cells reactive with the intact AChR plus T cells reactive with purified AChR subunits (α, β, γ, δ) were transferred and antigen-challenged in immunologically naive recipient rats; the serum anti-AChR antibody produced was assessed by radioimmunoassay for differences in titers and by isoelectric focusing for differences in clonal heterogeneity as a function of the subunit specificity of T cells transferred. In addition, rats receiving different sources of AChR or AChR subunit-reactive T cells were examined for AChR-dependent muscle dysfunction. The results indicated a clear reduction in anti-AChR antibody concentrations and clonal heterogeneity in recipient rats receiving T cells of specificities restricted to individual subunits. However, except for a clear relationship between serum anti-AChR antibody concentration and disease induction, no particular AChR subunit-reactive helper T cell specificity appeared to preferentially cause muscle dysfunction. We conclude that if such relationships exists, T cells with specificities more restricted than those described here will have to be used.

Original languageEnglish (US)
Pages (from-to)17-34
Number of pages18
JournalJournal of Neuroimmunology
Volume17
Issue number1
DOIs
StatePublished - 1987

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T-Cell Antigen Receptor Specificity
Cholinergic Receptors
Antibodies
Helper-Inducer T-Lymphocytes
T-Lymphocytes
Muscles
Isoelectric Focusing
Serum
Antibody Formation
Radioimmunoassay
B-Lymphocytes

Keywords

  • Acetylcholine receptor
  • Autoantibody
  • Muscle function
  • Myasthenia gravis
  • T cell specificity

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Clinical Neurology
  • Neurology

Cite this

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abstract = "Adoptive secondary anti-acetylcholine receptor (AChR) antibody responses were examined in rats to evaluate the influence of helper T cell specificity on the nature and disease-causing potential of antibody produced. Mixtures of B cells reactive with the intact AChR plus T cells reactive with purified AChR subunits (α, β, γ, δ) were transferred and antigen-challenged in immunologically naive recipient rats; the serum anti-AChR antibody produced was assessed by radioimmunoassay for differences in titers and by isoelectric focusing for differences in clonal heterogeneity as a function of the subunit specificity of T cells transferred. In addition, rats receiving different sources of AChR or AChR subunit-reactive T cells were examined for AChR-dependent muscle dysfunction. The results indicated a clear reduction in anti-AChR antibody concentrations and clonal heterogeneity in recipient rats receiving T cells of specificities restricted to individual subunits. However, except for a clear relationship between serum anti-AChR antibody concentration and disease induction, no particular AChR subunit-reactive helper T cell specificity appeared to preferentially cause muscle dysfunction. We conclude that if such relationships exists, T cells with specificities more restricted than those described here will have to be used.",
keywords = "Acetylcholine receptor, Autoantibody, Muscle function, Myasthenia gravis, T cell specificity",
author = "Yeh, {Trai Ming} and Krolick, {Keith A}",
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AU - Krolick, Keith A

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AB - Adoptive secondary anti-acetylcholine receptor (AChR) antibody responses were examined in rats to evaluate the influence of helper T cell specificity on the nature and disease-causing potential of antibody produced. Mixtures of B cells reactive with the intact AChR plus T cells reactive with purified AChR subunits (α, β, γ, δ) were transferred and antigen-challenged in immunologically naive recipient rats; the serum anti-AChR antibody produced was assessed by radioimmunoassay for differences in titers and by isoelectric focusing for differences in clonal heterogeneity as a function of the subunit specificity of T cells transferred. In addition, rats receiving different sources of AChR or AChR subunit-reactive T cells were examined for AChR-dependent muscle dysfunction. The results indicated a clear reduction in anti-AChR antibody concentrations and clonal heterogeneity in recipient rats receiving T cells of specificities restricted to individual subunits. However, except for a clear relationship between serum anti-AChR antibody concentration and disease induction, no particular AChR subunit-reactive helper T cell specificity appeared to preferentially cause muscle dysfunction. We conclude that if such relationships exists, T cells with specificities more restricted than those described here will have to be used.

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