Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR

被引：51

作者：

Poussin, MA ^{[1
]}

Goluszko, E ^{[1
]}

Hughes, TK ^{[1
]}

Duchicella, SI ^{[1
]}

Christadoss, P ^{[1
]}

机构：

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

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2000年 / 111卷 / 1-2期

关键词：

autoimmunity; myasthenia gravis; IL-10; IL-10 gene knockout; immunomodulation;

D O I：

10.1016/S0165-5728(00)00385-4

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. LL-IO KO mice had a Lower incidence and severity of EARAG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5(+)CD19(+) population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies. (C) 2000 Published by Elsevier Science B.V.

引用

页码：152 / 160

页数：9

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