IFN-α treatment suppresses the development of experimental autoimmune myasthenia gravis

M. Shenoy, S. Baron, B. Wu, E. Goluszko, P. Christadoss

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

Myasthenia gravis (MG) is an Ab-mediated autoimmune neuromuscular disease and is linked to MHC class II β-chain polymorphism. Corticosteroids and azathioprine are the primary immunosuppressive drugs used in the treatment of MG. These drugs have significant side effects and have limited efficacy. Therefore, drugs with fewer side effects and greater efficacy are being sought. IFN-α is a potent immunomodulator and has been shown to down- regulate MHC class II expression on lymphoid cells. MHC class II expression is critical for the development of experimental autoimmune myasthenia gravis (EAMG). Because of the immunomodulating effects of IFN-α and its effect on the MHC class II expression, we tested the therapeutic efficacy of IFN-α on EAMG induced by immunization with acetylcholine receptor (AChR) in CFA. IFN- α (105 IU three times weekly for 5 wk) treatment started 1 wk after the second immunization with AChR in CFA, when autoimmunity to AChR is well established, reduced the incidence of clinical EAMG by more than 50% in two separate experiments (p = 0.04 and 0.008). Therefore, IFN-α could be a potential agent for the control of MG, and other Ab-mediated autoimmune diseases.

Original languageEnglish (US)
Pages (from-to)6203-6208
Number of pages6
JournalJournal of Immunology
Volume154
Issue number11
StatePublished - Jan 1 1995

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Shenoy, M., Baron, S., Wu, B., Goluszko, E., & Christadoss, P. (1995). IFN-α treatment suppresses the development of experimental autoimmune myasthenia gravis. Journal of Immunology, 154(11), 6203-6208.