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

被引：37

作者：

Christadoss, P ^{[1
]}

Goluszko, E ^{[1
]}

机构：

[1] Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2002年 / 122卷 / 1-2期

关键词：

myasthenia gravis; autoimmunity; cytokine; TNF receptor; therapy;

D O I：

10.1016/S0165-5728(01)00473-8

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

页码：186 / 190

页数：5

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