The differentiation of human TH-17 cells requires transforming growth factor-β and induction of the nuclear receptor RORγt
By N. Manel, D. Unutmaz, Dan R. Littman. Nature Immunology, 2008
958 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/2366ab77aa69af171e9a36881256df6d1b5a2988
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Citations in the corpus
- Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies. (2012, background): “Second, amplification of Th17 cells driven by IL-21 produced by Th17 cell themselves, probably with TGF-β.”
- The Balance of Th17 versus Treg Cells in Autoimmunity (2018, background): “The effect of IL-6 is bolstered by other proinflammatory cytokines, including IL-1β, IL-21, IL-23, and TNF-α [3,53,58].”
- Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from TH-17, TH1 and TH2 cells (2009, background): “However, transduction of RORC into naive human cells does not lead to the production of IL-22, which suggests a difference between humans and mice in the requirement for RORC in IL-22 productio”
- IL-17 and Th17 Cells. (2009, background): “Only when additional cytokines such as IL-6 plus IL-23 or IL21 are present is RORc relieved from inhibition, and then naive T cells can begin transcribing IL-17 (29).”