| First Author | Oleinika K | Year | 2018 |
| Journal | Nat Commun | Volume | 9 |
| Issue | 1 | Pages | 684 |
| PubMed ID | 29449556 | Mgi Jnum | J:257949 |
| Mgi Id | MGI:6119269 | Doi | 10.1038/s41467-018-02911-y |
| Citation | Oleinika K, et al. (2018) CD1d-dependent immune suppression mediated by regulatory B cells through modulations of iNKT cells. Nat Commun 9(1):684 |
| abstractText | 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 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 alpha-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. |
