Late Developmental Plasticity in the T Helper 17 Lineage

Academic Article

Abstract

  • Development of T helper (Th) 17 cells requires transforming growth factor (TGF)-β and interleukin (IL)-6 and is independent of the Th1 pathway. Although T cells that produce interferon (IFN)-γ 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-γ-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-β for sustained expression of IL-17F and IL-17A. In the absence of TGF-β, both IL-23 and IL-12 acted to suppress IL-17 and enhance IFN-γ 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. © 2009 Elsevier Inc. All rights reserved.
  • Published In

  • Immunity  Journal
  • Digital Object Identifier (doi)

    Author List

  • Lee YK; Turner H; Maynard CL; Oliver JR; Chen D; Elson CO; Weaver CT
  • Start Page

  • 92
  • End Page

  • 107
  • Volume

  • 30
  • Issue

  • 1