Cutting Edge: An In Vivo Requirement for STAT3 Signaling in TH17 Development and TH17-Dependent Autoimmunity1

By T. Harris, J. Grosso, Hung-Rong Yen, H. Xin, M. Kortylewski, E. Albesiano, Edward L. Hipkiss, D. Getnet, Monica V. Goldberg, C. Maris and 4 more. Journal of Immunology, 2007

621 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/14643fde99b3e6a3d0bb1c4176f7aa549c8b1b6b

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In Immunology

1. A. Jetten
2. V. Kuchroo
3. J. O’Shea
4. D. Pardoll
5. S. Topalian
6. T. Korn
7. M. Oukka
8. Hua Yu

Citations in the corpus

• IL-17 and Th17 Cells. (2009, background): “In the follow-up study (9), they showed that IL-23 expands/generates IL-17-producing T cells that are capable of inducing EAE when adoptively transferred into naive wild-type mice.”
• Late Developmental Plasticity in the T Helper 17 Lineage (2009, background): “STAT3 plays a central role in Th17 development, coupling early IL-6 signaling to induction of IL-21, an autocrine factor implicated in the progression of Th17 development (Harris et al., 2007; Korn et al., 2007; Mathur et al., 2007; Nurieva et al., 2007; Yang et al., 2007; Zhou et al., 2007).”
• Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “Moreover, despite the link between STAT3 and models of Th17 cell-mediated diseases, our understanding of how STAT3 contributes to immunoregulation in terms of its gene targets is remarkably limited (Harris et al., 2007; Liu et al., 2008).”
• IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway (2009, background): “IL-6–induced Stat3 signaling in T cells is also critical in promoting Th17 cell differentiation and expression (Chen et al., 2006; Harris et al., 2007).”
• Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “Subsequent studies showed that, like RORγt, RORα is highly induced during Th17 cell differentiation in a STAT3-dependent manner [Yang et al., 2008d] (Figure 7).”
• The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment. (2009, neutral): “RORgt was probed as previously described (Harris et al., 2007).”
• Control of T(H)17/T(reg) balance by hypoxia-inducible factor 1. (2011, positive): “Intrigued by a potential link between the requirement for Stat3 in the TH17 program and our previous observation that HIF-1a is a target gene for activated Stat3 in tumor cells (Harris et al., 2007; Xu et al., 2005), we tested the hypothesis that HIF-1a plays a positive role in TH17 development.”