Neonatal tolerance to an immunodominant T cell reactivity does not confer resistance to EAMG induction in Lewis rats

Thomas E. Zoda, Kristi Brandon, Keith A. Krolick

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

The overall goal of this study was to determine, during induction of experimental autoimmune myasthenia gravis (EAMG) in Lewis rats, the relative importance of acetylcholine receptor (AChR)-reactive helper T cells associated with one particular immunodominant fine specificity. Thus, experiments presented below were designed to evaluate the immunopathological role played by helper T cells with reactivity against the AChR alpha subunit region associated with amino acid residues 100-116 (i.e., α100-116); in particular, the relationship between T cell reactivity with this specificity and disease induction was assessed. In order to examine the importance of this T cell reactivity, Lewis rat neonates were made T cell tolerant to a synthetic peptide α100-116 and subsequently evaluated for anti-AChR antibody production and resulting neuromuscular dysfunction. Results indicated that although T cell reactivity against the α100-116 peptide could be effectively removed from the Lewis T cell repertoire, tolerized Lewis rats immunized with AChR could undergo an active anti-AChR antibody response that produced symptoms of EAMG. Thus, other AChR T cell reactivities appeared capable of providing adequate help to B cells leading to production of anti-AChR antibodies with pathogenic potential.

Original languageEnglish (US)
Pages (from-to)35-44
Number of pages10
JournalJournal of Neuroimmunology
Volume57
Issue number1-2
DOIs
StatePublished - Mar 1995

Keywords

  • EAMG
  • Neonatal tolerance
  • T cell immunodominance

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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