A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

By Heon Park, Zhaoxia Li, Xuexian O. Yang, S. Chang, R. Nurieva, Yihong Wang, Ying Wang, Leroy Hood, Zhou Zhu, Qiang Tian and 1 more. Nature Immunology, 2005

4,711 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/ad9a84c9b8392aa3fa70ed61c8b1ec1bf1698354

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. D. Cua
2. A. Jetten
3. C. Dong
4. Dan R. Littman
5. V. Kuchroo
6. C. Weaver
7. J. Kolls
8. Christopher A. Hunter

In Pathology and Forensic Medicine

1. D. Cua
2. Dan R. Littman
3. V. Kuchroo
4. C. Weaver
5. Y. Iwakura
6. E. Bettelli
7. H. Ishigame
8. L. Harrington

Citations in the corpus

• IL-17 and Th17 Cells. (2009, background): “On the basis of this and other studies, investigators proposed that IL-17-producing T cells are a distinct T helper cell subset, which was named Th17 cells (9, 18, 19).”
• Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17–producing human T helper cells (2007, neutral): “dtd" [ ]> The T H -17 lineage of effector CD4 + T helper lymphocytes produces interleukin 17 (IL-17”
• Interleukin 23 receptor is essential for terminal differentiation of effector T helper type 17 cells in vivo (2009, neutral): “, although other studies have reported no STAT4 involvemen”
• Differential roles of interleukin-17A and -17F in host defense against mucoepithelial bacterial infection and allergic responses. (2009, background): “Overexpression of IL-17F or IL-17A in the lungs leads to increased proinflammatory cytokine and chemokine expression, resulting in inflammation associated with neutrophil infiltration (Hurst et al., 2002; Oda et al., 2005; Park et al., 2005; Yang et al., 2008).”
• Differentiation of Effector CD4 T Cell Populations (2010, neutral): “RORγt/RORα—Th17 cells do not express GATA3 or T-bet (19, 20); instead, they express high levels of RORγt (90).”
• A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage (2007, background): “When treatment was started at the peak of paralysis, disease progression was attenuate”
• Interleukin 17–producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice (2008, background): “Studies indicate that IL-17–producing T-helper (T H -17) cells constitute a distinct CD4 + T helper effector cell population that differs in function and phenotype from the classical T helper type 1 (T H 1) and T H 2 population”
• Th17 cells in human disease (2008, background): “Th1 and Th2 cells are known to antagonize each other, and not surprisingly, IL-12, IFN-g, and IL-4 can inhibit Th17 differentiation in both mouse and human (2, 3, 17, 19, 20, 25, 26).”
• Identification of an IL-17–producing NK1.1neg iNKT cell population involved in airway neutrophilia (2007, positive): “Knowing that both cytokines are potent inhibitors of IL-17 production (22, 23), we examined how this activity was aff ected when endogenous IFN-γ and/or IL-4 production was abolished in genetically modifi ed IFN-γ−/− mice and/or in the presence of neutralizing anti–IL-4 mAbs.”