Treatment of experimental autoimmune myasthenia gravis with recombinant human tumor necrosis factor receptor Fc protein

Premkumar Christadoss, Elzbieta Goluszko

Research output: Contribution to journalArticle

43 Scopus citations


Lymphotoxin-α (TNF-β) and TNF receptor p55 gene knockout mice are resistant to the development of antibody and complement mediated experimental autoimmune myasthenia gravis (EAMG), suggesting a possible role of TNF in mediating EAMG. Therefore, we tested the hypothesis that blocking the functional interaction of TNF with their receptors by soluble recombinant human TNFR:Fc would suppress the ongoing clinical EAMG. Recombinant human TNFR:Fc administered daily for 2 weeks to C57BL6 mice with ongoing clinical EAMG significantly improved clinical EAMG when compared with placebo-treated mice. A clinical trial of selected myasthenia gravis patients with recombinant human TNFR:Fc could be attempted.

Original languageEnglish (US)
Pages (from-to)186-190
Number of pages5
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Jan 29 2002



  • Autoimmunity
  • Cytokine
  • Myasthenia gravis
  • TNF receptor
  • Therapy

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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