Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells.

By Zhi Chen, A. Laurence, Y. Kanno, Margit Pacher-zavisin, B. Zhu, C. Tato, A. Yoshimura, L. Hennighausen, J. O’Shea. Proceedings of the National Academy of Sciences of the United States of America, 2006

712 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/8f9f456b2299c677903ee5565aa6352978574afe

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. A. Jetten
2. W. E. Paul
3. Jinfang Zhu
4. D. Cua
5. Dan R. Littman
6. C. Dong
7. V. Kuchroo
8. J. O’Shea

In Oncology

1. V. Kuchroo
2. J. O’Shea
3. Hua Yu
4. D. Pardoll
5. Christopher A. Hunter
6. D. Cua
7. A. Laurence
8. Dan R. Littman

Citations in the corpus

• IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway (2009, background): “Similar to IL-23, IL-17 expression is also regulated by Stat3 (Chen et al., 2006), which is an oncogene persistently activated in tumor cells and tumor stromal cells, promoting tumor cell survival, proliferation, JEM VOL. 206, July 6, 2009 1459 BRIEF DEFINITIVE REPORT RESULTS AND DISCUSSION Th17…”
• A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses (2009, neutral): “Stat3 transduces signals from numerous growth factor and cytokine receptors, is constitutively activated in diverse cancers and is absolutely required for T H 17 cell generation while simultaneously negatively regulating T H 1-mediated inflammatio”
• IL-17 family cytokines and the expanding diversity of effector T cell lineages. (2007, background): “IL-23 also induces IL-17 via STAT3, and loss of SOCS3 increases binding of STAT3 to the IL-17 promoter and enhances IL-17 production in response to IL-6 and TGF-β (124).”
• Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation. (2007, methodology): “As indicated above, by using chromatin immunoprecipitation (ChIP), we have previously shown that STAT3 directly binds to the Il17a promoter and that STAT5 directly binds the Foxp3 promoter (Chen et al., 2006; Yao et al., 2007).”
• Peripheral CD4 T cell differentiation regulated by networks of cytokines and transcription factors (2010, background): “Both RORct and STAT3 bind to multiple sites in the Il17a ⁄ Il17f locus including the promoters of these cytokines (80, 82, 164, 165).”
• STATs in cancer inflammation and immunity: a leading role for STAT3 (2009, neutral): “STAT3 also mediates T regulatory cell expansion in tumours and is necessary for the development of T H 17 T cells”
• Plasticity of CD4+ T cell lineage differentiation. (2009, background): “Stat3 binds to the Il17 locus to direct its transcription, presumably through cooperative activity with RORgt (Chen et al., 2006).”
• Cytokine signaling modules in inflammatory responses. (2008, background): “However, because IL-10 regulates its own production by Stat3 (Cheng et al., 2003; Staples et al., 2007), the feed-forward loop via Stat3 also fails.”
• Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “Inversely, deficiency in suppressor of cytokine signaling 3 (SOCS3), a negative regulator of STAT3 activity, enhances Th17 differentiation [Chen et al., 2006].”
• Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “Accordingly, we and others have shown that STAT3 plays a critical role in the differentiation of CD4+ T cells into Th17 cells (Chen et al., 2006; Laurence et al., 2007; Mathur et al., 2007; Wei et al., 2007; Yang et al., 2007).”