Cutting edge: Discrete functions of mTOR signaling in invariant NKT cell development and NKT17 fate decision.

ABSTRACT: Invariant NKT (iNKT) cells recently were classified into NKT1, NKT2, and NKT17 lineages with distinct transcription factor and cytokine profiles, but the mechanisms underlying such fate decisions remain elusive. In this article, we report crucial roles for mechanistic target of rapamycin (mTOR) signaling, especially mTORC2, in iNKT cell development and fate determination of NKT17 cells. Loss of Rictor, an obligatory component of mTORC2, decreased thymic and peripheral iNKT cells, which was associated with defective survival. Strikingly, Rictor deficiency selectively abolished the NKT17 lineage, as indicated by a marked reduction in RORγt and IL-17 expression. Moreover, deletion of phosphatase and tensin homolog (Pten) upregulated mTORC2 activity and enhanced NKT17 generation, but concomita

SUBMITTER: Wei J 

PROVIDER: S-EPMC4201958 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature