Myocytes respond in vivo to an antibody reactive with the acetylcholine receptor by upregulating interleukin-15: An interferon-gamma activator with the potential to influence the severity and course of experimental myasthenia gravis

Timothy Stegall, Keith A. Krolick

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

The monoclonal antibody, mAb35, which binds the main immunogenic region of the post-junctional muscle receptor for acetylcholine (AChR), results in contractile dysfunction and symptoms of experimental myasthenia gravis (EAMG). As described below, exposure to mAb35 also results in the production by muscle of increased levels of the interferon-gamma (IFN-γ)-activating cytokine, interleukin-15. This effect is accompanied by the increased trafficking of leukocytes through muscle, some that produce IFN-γ. These observations may be relevant to the induction of disease symptoms since numerous reports from other investigators indicate that IFN-γ may play a pivotal role in this disease process.

Original languageEnglish (US)
Pages (from-to)377-386
Number of pages10
JournalJournal of Neuroimmunology
Volume119
Issue number2
DOIs
StatePublished - Oct 1 2001

Keywords

  • Experimental myasthenia gravis
  • IFN-gamma
  • IL-15
  • IL-4
  • Muscle

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Fingerprint Dive into the research topics of 'Myocytes respond in vivo to an antibody reactive with the acetylcholine receptor by upregulating interleukin-15: An interferon-gamma activator with the potential to influence the severity and course of experimental myasthenia gravis'. Together they form a unique fingerprint.

  • Cite this