B cells regulate autoimmunity by provision of IL-10

被引：1361

作者：

Fillatreau, S ^{[1
]}

Sweenie, CH ^{[1
]}

McGeachy, MJ ^{[1
]}

Gray, D ^{[1
]}

Anderton, SM ^{[1
]}

机构：

[1] Univ Edinburgh, Inst Cell Anim & Populat Biol, Edinburgh EH9 3JT, Midlothian, Scotland

来源：

NATURE IMMUNOLOGY | 2002年 / 3卷 / 10期

基金：

英国惠康基金; 英国医学研究理事会;

关键词：

D O I：

10.1038/ni833

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

To assess the importance of B cell control of T cell differentiation, we analyzed the course of the T helper type 1 (T(H)1)-driven disease experimental autoimmune encephalomyelitis in mice with an altered B cell compartment. We found that recovery was dependent on the presence of autoantigen-reactive B cells. B cells from recovered mice produced interleukin 10 (IL-10) in response to autoantigen. With a bone marrow chimeric system, we generated mice in which IL-10 deficiency was restricted to B cells but not T cells. In the absence of IL-10 production by B cells, the proinflammatory type 1 immune response persisted and mice did not recover. These data show that B cell-derived IL-10 plays a key role in controlling autoimmunity.

引用

页码：944 / 950

页数：7

共 47 条

[1]

Incorporation of cells into an ELISA system enhances antigen-driven lymphokine detection [J].