Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis

被引：28

作者：

Goluszko, E ^{[1
]}

Deng, CS ^{[1
]}

Poussin, MA ^{[1
]}

Christadoss, P ^{[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：

autoimmunity; myasthenia gravis; TNF-alpha; lymphotoxin-alpha; TNF receptors;

D O I：

10.1016/S0165-5728(01)00474-X

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55(-/-) p75(-/-) mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG(1), IgG(2a), and IgG(2b) anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55(-/-) p75(-/-) mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

页码：85 / 93

页数：9

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