Subcutaneous administration of T-epitope sequences of the acetylcholine receptor prevents experimental myasthenia gravis

Peter I. Karachunski, Norma S. Ostlie, David K. Okita, Richard Garman, Bianca M. Conti-Fine

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Immunization with acetylcholine receptor (AChR) causes experimental myasthenia gravis (EMG). The s.c. administration to C57B1/6 mice of synthetic AChR CD4+ epitopes, before and during AChR immunization, reduced the epitope-specific CD4+ responses and the anti-AChR Ab synthesis, and prevented EMG. The s.c. administration of solubilized AChR had effects similar to those of peptide treatment. Sham-tolerized mice had only Th1 anti- AChR cells, whereas peptide-treated mice had also Th2 cells, and Th2-induced anti-peptide Ab. Established EMG was not affected by s.c. peptide treatment, whereas it worsened after s.c. administration of solubilized AChR.

Original languageEnglish (US)
Pages (from-to)108-121
Number of pages14
JournalJournal of Neuroimmunology
Volume93
Issue number1-2
DOIs
StatePublished - Jan 1 1999

Keywords

  • Acetylcholine receptor
  • Autoimmunity
  • Experimental myasthenia gravis
  • Subcutaneous tolerance
  • Th2 cells

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