Tbet or Continued RORγt Expression Is Not Required for Th17-Associated Immunopathology

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Tbet or Continued RORγt Expression Is Not Required for Th17-Associated Immunopathology

The discovery of Th17 cell plasticity, in which CD4(+) IL-17-producing Th17 cells give rise to IL-17/IFN-γ double-producing cells and Th1-like IFNγ(+) ex-Th17 lymphocytes, has raised questions regarding which of these cell types contribute to immunopathology during inflammatory diseases. In this study, we show using Helicobacter hepaticus-induced intestinal inflammation that IL-17A(Cre)- or Rag...

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IFNγ inhibits Th17 differentiation and function via Tbet-dependent and Tbet-independent mechanisms

The transcription factor Tbet is critical for the differentiation of Th1 CD4 T cells and is associated with the induction of multiple autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE). Herein, we demonstrate that Tbet suppresses IL-17A and Th17 differentiation both in vitro and in vivo in a cell-intrinsic manner, and that in fact, Tbet is not necessary for EAE induc...

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IL-6-mediated Th17 differentiation through RORγt is essential for the initiation of experimental autoimmune myocarditis.

AIMS Interleukin (IL)-17-producing helper T (Th17) cells have been proposed to participate in the pathogenesis of chronic inflammation, such as autoimmune myocarditis. IL-6 gene ablation confers the resistance to experimental autoimmune myocarditis (EAM). In this study, we have addressed the pathological roles of IL-6 in the regulation of Th17 cells in EAM. METHODS AND RESULTS To induce EAM, ...

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ژورنال

عنوان ژورنال: The Journal of Immunology

سال: 2016

ISSN: 0022-1767,1550-6606

DOI: 10.4049/jimmunol.1600137