| First Author | Lee YK | Year | 2009 |
| Journal | Immunity | Volume | 30 |
| Issue | 1 | Pages | 92-107 |
| PubMed ID | 19119024 | Mgi Jnum | J:143729 |
| Mgi Id | MGI:3828878 | Doi | 10.1016/j.immuni.2008.11.005 |
| Citation | Lee YK, et al. (2009) Late developmental plasticity in the T helper 17 lineage. Immunity 30(1):92-107 |
| abstractText | Development of T helper (Th) 17 cells requires transforming growth factor (TGF)-beta and interleukin (IL)-6 and is independent of the Th1 pathway. Although T cells that produce interferon (IFN)-gamma are a recognized feature of Th17 cell responses, mice deficient for STAT4 and T-bet-two prototypical Th1 transcription factors-are protected from autoimmunity associated with Th17 pathogenesis. To examine the fate and pathogenic potential of Th17 cells and origin of IFN-gamma-producing T cells that emerge during Th17 immunity, we developed IL-17F reporter mice that identify cells committed to expression of IL-17F and IL-17A. Th17 cells required TGF-beta for sustained expression of IL-17F and IL-17A. In the absence of TGF-beta, both IL-23 and IL-12 acted to suppress IL-17 and enhance IFN-gamma production in a STAT4- and T-bet-dependent manner, albeit with distinct efficiencies. These results support a model of late Th17 developmental plasticity with implications for autoimmunity and host defense. |
