Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells

Mathilde A. Poussin, Claudette L. Fuller, Elzbieta Goluszko, Victor E. Reyes, Vivian L. Braciale, Premkumar Christadoss

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Class II MHC mutant bm12 mice have an increased resistance to experimental autoimmune myasthenia gravis (EAMG) compared to C57BL/6 mice. In vitro, this relative resistance was mainly associated with a reduced cytokine response to acetylcholine receptor (AChR) and its dominant pathogenic peptide α146-162, whereas the response to the epitope α111-126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or α146-162 peptide, but not α111-126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-γ and IL-10 release, and intracellular calcium mobilization by α146-162-specific T cells.

Original languageEnglish (US)
Pages (from-to)104-110
Number of pages7
JournalJournal of Neuroimmunology
Volume134
Issue number1-2
DOIs
StatePublished - Jan 1 2003

Keywords

  • Antigen presentation
  • Autoimmunity
  • Class II MHC
  • Cytokines
  • Mouse model
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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