Interleukin-12 enhances clinical experimental autoimmune myasthenia gravis in susceptible but not resistant mice

Sheela Sitaraman, Dennis W. Metzger, Robert J. Belloto, Anthony J. Infante, Katherine A. Wall

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

Experimental autoimmune myasthenia gravis (EAMG) is induced by antibodies against the nicotinic acetylcholine receptor (AChR). Studies indicate a role for interferon-γ (IFN-γ) in EAMG. We examined the effect of IL-12, a major inducer of IFN-γ production, on EAMG in C57BL/6 mice. Five doses of IL-12 accelerated and enhanced clinical disease in AChR-immunized mice. Control B6 mice, IFN-γ gene-knockout mice, and EAMG-resistant bm12 mice showed no enhancement of disease. Shifting to a Th1-type antibody isotype distribution was insufficient to cause disease. Other factors, such as direct effects of Th1 cytokines on muscle tissue, may be involved in EAMG susceptibility. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)73-82
Number of pages10
JournalJournal of Neuroimmunology
Volume107
Issue number1
DOIs
StatePublished - Jul 10 2000

Keywords

  • Autoantibodies
  • Cytokines
  • Experimental autoimmune myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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