| First Author | Sklarz T | Year | 2017 |
| Journal | Eur J Immunol | Volume | 47 |
| Issue | 3 | Pages | 516-526 |
| PubMed ID | 28078715 | Mgi Jnum | J:246561 |
| Mgi Id | MGI:5922756 | Doi | 10.1002/eji.201646343 |
| Citation | Sklarz T, et al. (2017) mTORC2 regulates multiple aspects of NKT-cell development and function. Eur J Immunol 47(3):516-526 |
| abstractText | Invariant NKT (iNKT) cells bridge innate and adaptive immunity by rapidly secreting cytokines and lysing targets following TCR recognition of lipid antigens. Based on their ability to secrete IFN-gamma, IL-4 and IL-17A, iNKT-cells are classified as NKT-1, NKT-2, and NKT-17 subsets, respectively. The molecular pathways regulating iNKT-cell fate are not fully defined. Recent studies implicate Rictor, a required component of mTORC2, in the development of select iNKT-cell subsets, however these reports are conflicting. To resolve these questions, we used Rictorfl/fl CD4cre+ mice and found that Rictor is required for NKT-17 cell development and normal iNKT-cell cytolytic function. Conversely, Rictor is not absolutely required for IL-4 and IFN-gamma production as peripheral iNKT-cells make copious amounts of these cytokines. Overall iNKT-cell numbers are dramatically reduced in the absence of Rictor. We provide data indicating Rictor regulates cell survival as well as proliferation of developing and mature iNKT-cells. Thus, mTORC2 regulates multiple aspects of iNKT-cell development and function. |
