Tbet or Continued RORγt Expression Is Not Required for Th17-Associated Immunopathology
نویسندگان
چکیده
منابع مشابه
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...
متن کاملIFNγ 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...
متن کاملIL-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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Maspin (SERPINB5) is accepted as an important tumour suppressor lost in many cancers. Consistent with a critical role in development or differentiation maspin knockout mice die during early embryogenesis, yet clinical data conflict on the prognostic utility of maspin expression. Here to reconcile these findings we made conditional knockout mice. Surprisingly, maspin knockout embryos develop int...
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ژورنال
عنوان ژورنال: The Journal of Immunology
سال: 2016
ISSN: 0022-1767,1550-6606
DOI: 10.4049/jimmunol.1600137