Treatment of experimental autoimmune myasthenia gravis with recombinant human tumor necrosis factor receptor Fc protein
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Updated: Oct 3, 2026

Preparing T Cell Growth Factor from Rat Splenocytes
Published on: October 31, 2007
Premkumar Christadoss1, Elzbieta Goluszko
1Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Boulevard, 3.142 MRB, Galveston, TX 77555-1070, USA. pchrista@utmb.edu
Abstract:
Lymphotoxin-alpha (TNF-beta) 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.
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