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Immunity. 2009 Jan 16;30(1):92-107. doi: 10.1016/j.immuni.2008.11.005.

Late developmental plasticity in the T helper 17 lineage.

Author information

1
Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

Abstract

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.

PMID:
19119024
PMCID:
PMC3607320
DOI:
10.1016/j.immuni.2008.11.005
[Indexed for MEDLINE]
Free PMC Article

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