Interleukin-4 deficiency facilitates development of experimental myasthenia gravis and precludes its prevention by nasal administration of CD4+-epitope sequences of the acetylcholine receptor

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

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38 Scopus citations

Abstract

Immunization with acetylcholine receptor (AChR) causes experimental myasthenia gravis (EMG). We investigated EMG in interleukin (IL)-4 knock out B6 (KO) mice that lack Th2 cells. EMG was more frequent in KO than in wild type B6 mice. KO and B6 mice developed similar amounts of anti-AChR antibodies. They were IgG2a and IgG2b in KO mice, IgG1 and IgG2b in B6 mice. CD4+ cells from KO and B6 mice recognized the same AChR epitopes. Nasal administration of synthetic AChR CD4+ epitopes reduced antibody synthesis and prevented EMG in B6, not in KO mice. Thus, Th2 cells may have protective functions in EMG.

Original languageEnglish (US)
Pages (from-to)73-84
Number of pages12
JournalJournal of Neuroimmunology
Volume95
Issue number1-2
DOIs
StatePublished - Mar 1 1999

Keywords

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

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