| Literature DB >> 11777558 |
Premkumar Christadoss1, Elzbieta Goluszko.
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.Entities:
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Year: 2002 PMID: 11777558 DOI: 10.1016/s0165-5728(01)00473-8
Source DB: PubMed Journal: J Neuroimmunol ISSN: 0165-5728 Impact factor: 3.478