The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.

By I. Ivanov, Brent S. McKenzie, Liang Zhou, C. Tadokoro, A. Lepelley, J. Lafaille, D. Cua, Dan R. Littman. Cell, 2006

2,656 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c33fadd9506663d893cb0dfdb6952b8eedd620a8

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1. K. Honda
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3. Jinfang Zhu
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5. Hsin-jung Wu
6. Dan R. Littman
7. Ryan M. O’Connell
8. W. E. Paul

Citations in the corpus

• Critical regulation of early Th17 cell differentiation by IL-1 signaling (2009, background): “We found that Th17 cells expressed higher amounts of IL-1R1 mRNA, which was dependent on STAT3, RORa, and RORgt.”
• Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17–producing T cell responses (2007, unknown): “T H -17 cells are present in appreciable numbers in the lamina propri”
• CD4+T Cells: Differentiation and Functions (2012, unknown): “Downstream TGFβ signaling pathway in the presence of IL6 leads to the activation of RORγt [66, 67].”
• Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis. (2008, background): “Although EAE could still occur in IL-17 knockout mice, the disease was heavily attenuated,(8) and mice deficient for the key transcription factor for differentiation of TH17 cells, the orphan nuclear receptor ROR t, showed a mild EAE course and a delayed onset.(9) However, although CD4 FoxP3 regulat”
• T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma. (2008, unknown): “expressed in TH17 cells (data not shown), RORγ, in particular the RORγt isoform, was previously identified as a critical transcription factor regulating TH17 differentiation (Ivanov et al., 2006).”
• The differentiation of human TH-17 cells requires transforming growth factor-β and induction of the nuclear receptor RORγt (2008, unknown): “RORγt is sufficient to direct IL-17 expression in activated mouse T cell”
• Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death (2007, unknown): “Although the factors that regulate the lineage commitment and differentiation of T H 1, T H 2 and T H -17 cells are relatively well understoo”
• The development of inflammatory TH-17 cells requires interferon-regulatory factor 4 (2007, unknown): “RORγt (a nuclear hormone receptor) has been identified as a transcription factor important for T H -17 developmen”
• Nuclear receptor transrepression pathways that regulate inflammation in macrophages and T cells (2010, unknown): “A striking example is provided by retinoic acid receptor-related orphan receptor-γt ( RORγt ), an isoform of RORγ (also known as NR1F3) that arises from an alternative T cell-specific promoter and is required, in combination with other factors, for the differentiation of T H 17 cell”