| First Author | Wu J | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 9 | Pages | e75202 |
| PubMed ID | 24073253 | Mgi Jnum | J:207526 |
| Mgi Id | MGI:5559083 | Doi | 10.1371/journal.pone.0075202 |
| Citation | Wu J, et al. (2013) Diacylglycerol kinase zeta positively controls the development of iNKT-17 cells. PLoS One 8(9):e75202 |
| abstractText | Invariant natural killer T (iNKT) cells play important roles in bridging innate and adaptive immunity via rapidly producing a variety of cytokines. A small subset of iNKT cells produces IL-17 and is generated in the thymus during iNKT-cell ontogeny. The mechanisms that control the development of these IL-17-producing iNKT-17 cells (iNKT-17) are still not well defined. Diacylglycerol kinase zeta (DGKzeta) belongs to a family of enzymes that catalyze the phosphorylation and conversion of diacylglycerol to phosphatidic acid, two important second messengers involved in signaling from numerous receptors. We report here that DGKzeta plays an important role in iNKT-17 development. A deficiency of DGKzeta in mice causes a significant reduction of iNKT-17 cells, which is correlated with decreased RORgammat and IL-23 receptor expression. Interestingly, iNKT-17 defects caused by DGKzeta deficiency can be corrected in chimeric mice reconstituted with mixed wild-type and DGKzeta-deficient bone marrow cells. Taken together, our data identify DGKzeta as an important regulator of iNKT-17 development through iNKT-cell extrinsic mechanisms. |
