期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-02911-y
关键词
-
资金
- UK Medical Research Council studentship [G0900950]
- European Community's Seventh Framework Programme [HEALTH-F2-2013-602114]
- Arthritis Research UK Foundation fellowship [21141]
- Wellcome Trust [097259/Z/11/Z]
- Arthritis Research UK studentship [21257]
- Nuffield Foundation Oliver Bird Rheumatism Program studentship
- Versus Arthritis [21141] Funding Source: researchfish
Regulatory B cells (Breg) express high levels of CD1d that presents lipid antigens to invariant natural killer T (iNKT) cells. The function of CD1d in Breg biology and iNKT cell activity during inflammation remains unclear. Here we show, using chimeric mice, cell depletion and adoptive cell transfer, that CD1d-lipid presentation by Bregs induces iNKT cells to secrete interferon (IFN)-gamma to contribute, partially, to the downregulation of T helper (Th) 1 and Th17adaptive immune responses and ameliorate experimental arthritis. Mice lacking CD1d-expressing B cells develop exacerbated disease compared to wild-type mice, and fail to respond to treatment with the prototypical iNKT cell agonist a-galactosylceramide. The absence of lipid presentation by B cells alters iNKT cell activation with disruption of metabolism regulation and cytokine responses. Thus, we identify a mechanism by which Bregs restrain excessive inflammation via lipid presentation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据