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CD1d-dependent immune suppression mediated by regulatory B cells through modulations of iNKT cells.


ABSTRACT: 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)-? to contribute, partially, to the downregulation of T helper (Th)1 and Th17-adaptive 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 ?-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.

SUBMITTER: Oleinika K 

PROVIDER: S-EPMC5814456 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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CD1d-dependent immune suppression mediated by regulatory B cells through modulations of iNKT cells.

Oleinika K K   Rosser E C EC   Matei D E DE   Nistala K K   Bosma A A   Drozdov I I   Mauri C C  

Nature communications 20180215 1


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)-γ to contribute, partially, to the downregulation of T helper (Th)1 and Th17-adaptive immune responses and amelio  ...[more]

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