Journal
NATURE COMMUNICATIONS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-02911-y
Keywords
-
Categories
Funding
- 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
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available