Essential autocrine regulation by IL-21 in the generation of inflammatory T cells

By R. Nurieva, Xuexian O. Yang, G. Martinez, Yongliang Zhang, Athanasia D. Panopoulos, Li Ma, K. Schluns, Qiang Tian, S. Watowich, A. Jetten and 1 more. Nature, 2007

1,645 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/31ab1ae14931f26e596470722dac55bd332349fa

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In Immunology

1. W. E. Paul
2. Shizuo Akira
3. A. Jetten
4. Jinfang Zhu
5. D. Cua
6. C. Dong
7. R. Flavell
8. Dan R. Littman

Citations in the corpus

• New insights into the regulation of T cells by γc family cytokines (2009, neutral): “The presence of either IL-6 or IL-21 during priming with TGFβ subverts T cell differentiation from the FOXP3-directed T Reg cell pathway to the T H 17 cell pathway through the induction of expression of the orphan nuclear receptor retinoic acid receptor-related orphan receptor-γt (RORγt; also known”
• Critical regulation of early Th17 cell differentiation by IL-1 signaling (2009, background): “…Th17 cell priming cytokine—it can not only initiate Th17 cell differentiation and downregulate Foxp3 expression, but it also has been shown to allow CD4+ T cells to produce IL-21 (Nurieva et al., 2007; Zhou et al., 2007) and respond to IL-1 and IL-23 (Yang et al., 2007; Zhou et al., 2007).”
• Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “As previously reported, we found that STAT3 bound to the Il17a and Il21 promoters (Figure 4A) (Chen et al., 2006; Nurieva et al., 2007; Wei et al., 2007).”
• T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma. (2008, background): “STAT3 is necessary for IL-6 induction of IL-21 expression and is required for IL-21-mediated TH17 differentiation (Nurieva et al., 2007).”
• Cytokine signaling modules in inflammatory responses. (2008, background): “Th17 cells can be generated from naive CD4+ T cells by IL-6 and TGF-b but can also produce another cytokine IL-21, which promotes IL-17 production in an autocrine-paracrine manner (Nurieva et al., 2007; Zhou et al., 2007).”
• Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “…are reciprocally regulated, involving several positive and negative regulatory networks [Bettelli et al., 2008; Dong, 2008; Furuzawa-Carballeda et al., 2007; Ivanov et al., 2007; Laurence and O'Shea, 2007; Nurieva et al., 2007; Weaver et al., 2007; Zheng and Rudensky, 2007; Zhou et al., 2008].”
• IL-21 regulates germinal center B cell differentiation and proliferation through a B cell–intrinsic mechanism (2010, background): “Although there is uncertainty about the stringency of the requirement for IL-21 in the formation of Th17 in vivo (Coquet et al., 2008; Sonderegger et al., 2008), it is possible that this T cell subset may influence GC function, as IL-17 has been shown to influence GC B cell activity in at least one ”
• Specific microbiota direct the differentiation of Th17 cells in the mucosa of the small intestine (2008, neutral): “Mice deficient for IL-23 (Il23a / ) also had Th17 cells in the SI LP, consistent with the notion that IL-23 may be required mostly for the maintenance or expansion of this population (Weaver et al., 2006, 2007).”
• Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5 (2008, background): “Although we detected only interferon-γ (IFN-γ)-producing cells in cocultures of OT-II T cells and LPS-stimulated SPDCs, we detected both IL-17- and IFN-γ-producing cells in cocultures of OT-II T cells and CD11c hi CD11b hi LPDCs; the numbers of IL-17- and IFN-γ-producing OT-II cells were further in”
• The biological functions of T helper 17 cell effector cytokines in inflammation. (2008, neutral): “Most recently , however, several groups simultaneously identified that IL-21 was also produced by Th17 cells and exerted critical functions in Th17 cell development (Korn et al., 2007; Nurieva et al., 2007; Zhou et al., 2007).”
• IL-21 acts directly on B cells to regulate Bcl-6 expression and germinal center responses (2010, background): “…there was a 72% reduction in HEL3Xhi-binding GC B cells (P = 0.035) 10 d Th17 cell formation, it is possible that a role for IL-21 would become more apparent in IL-6–deficient mice (Korn et al., 2007; Nurieva et al., 2007; Zhou et al., 2007; Coquet et al., 2008; Sonderegger et al., 2008).”
• The cytokine network in asthma and chronic obstructive pulmonary disease. (2008, background): “TGF-β also has immunoregulatory effects that are largely mediated through Tregs through the induction of FOXP3, resulting in suppression of Th1 and Th2 cells (73).”
• Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity. (2009, background): “We have shown that IL-1b and IL-23 can induce IL-17 and IL-21 expression in gd T cells, and it has already been reported that IL-21 together with TGF-b or IL-23 can stimulate IL-17 production by CD4+ T cells (Korn et al., 2007; Nurieva et al., 2007; Zhou et al., 2007).”
• Innate and adaptive interleukin-22 protects mice from inflammatory bowel disease (2008, background): “Differentiation in mice appears to be directed by the presence of both transforming growth factor-beta (TGF-b) and inflammatory cytokines, such as IL-6 or IL-21, that activate Stat3 signaling pathways in the T cells (Korn et al., 2007; Nurieva et al., 2007; Veldhoen et al., 2006).”