TH17 cells in development: an updated view of their molecular identity and genetic programming

By C. Dong. Nature reviews. Immunology, 2008

1,142 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a8fdd24192616f34e3f067e92673321591e38f04

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Citations in the corpus

Global mapping of H3K4me3 and H3K27me3 reveals specificity and plasticity in lineage fate determination of differentiating CD4+ T cells. (2009, background): “IL-6, IL-21, and IL-23 all signal through Stat3, and in combination with TGFb-1 induce the transcription factors RORgt and RORa (Chen et al., 2006; Dong, 2008; Korn et al., 2007; Nurieva et al., 2007; Wei et al., 2007; Yang et al., 2008a; Zhou et al., 2007).”
NF-κB signaling in inflammation (2017, positive): “2,91,92 Deregulated activation of NF-κ B also contributes to aberrant survival of self-reactive B cells and production of auto-antibodies that contribute to the pathogenesis of RA.”
Control of T(H)17/T(reg) balance by hypoxia-inducible factor 1. (2011, positive): “TH17 and Treg cells share a common requirement for TGF-b in their differentiation requirements despite expressing distinct transcriptional regulators (RORgt versus Foxp3, respectively) and demonstrating opposing functions (inflammatory versus anti-inflammatory) (Bettelli et al., 2006; Dong, 2008; Li”
Orchestrating the orchestrators: chemokines in control of T cell traffic (2008, background): “IL-17-producing T helper cells CD4 + T cell populations that upregulate expression of the transcription factor RORγt can differentiate into T H -17 cells, an IL-17-producing CD4 + T cell population that differs in phenotype and function from T H 1 and T H 2 cell”
MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis (2009, background): “Interleukin 17 (IL-17)-producing T helper cells (T H -17 cells) have been identified as a distinct subset of effector helper T cells that are essential in clearing foreign pathogens and inducing tissue inflammation during autoimmune diseas”
Analysing biological pathways in genome-wide association studies (2010, methodology): “Applying pathway-based association approaches As an example of how biological pathways are involved in disease pathogenesis, we discuss a manually compiled pathway centred on interleukin (IL)-12 and IL-23 (Ref”
Epigenetic control of T-helper-cell differentiation (2009, background): “Transforming growth factor-β ( TGFβ ) inhibits T H 1- and T H 2-cell differentiation, and promotes regulatory T (T Reg )-cell and T H 17-cell lineage commitment by inducing the expression of the transcription factors forkhead box P3 (FOXP3) and retinoic-acid-receptor-related orphan receptor-γt ( ROR”
CD4+ T Cells Regulate Pulmonary Metastasis of Mammary Carcinomas by Enhancing Protumor Properties of Macrophages (2009, background): “, TH17 cells) that might also regulate chronic inflammation and promote tumor development when activated in the presence of TGF-b and IL-6, or IL-23 (Dong, 2008).”
Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “Neutralizing IL-17 with antibodies suppresses CNS autoimmune inflammation [Dong, 2008; Furuzawa-Carballeda et al., 2007; Huang et al., 2007; Korn et al., 2007b; Stockinger et al., 2007].”
Molecular antagonism and plasticity of regulatory and inflammatory T cell programs. (2008, background): “In addition to Th1 and Th2 cells (Dong and Flavell, 2000), a third subset of effector Th cells, Th17, has been identified; these produce IL-17, IL-17F, and IL-22 and regulate inflammatory responses by tissue cells (Dong, 2008).”
Dendritic-cell-based therapeutic cancer vaccines. (2013, background): “Th17 cells (Dong, 2008) exert either protumor or antitumor activity depending on the tissue environment in which they reside (reviewed inWei et al., 2012).”
Generation of follicular helper T cells is mediated by IL-21 but independent of TH1, TH2 or TH17 lineages (2008, background): “In addition to Th1 and Th2 cells (Dong and Flavell, 2000), Th17 cells, a third subset of Th cells, have been recently identified; Th17 cells produce interleukin-17 (IL-17), IL-17F, and IL-22 and regulate inflammatory responses by tissue cells (Dong, 2008).”
RORγt+ innate lymphoid cells regulate intestinal homeostasis by integrating negative signals from the symbiotic microbiota (2011, background): “, where activators of STAT3 such as IL-6, IL-21 and IL-23 (ref”
Critical regulation of early Th17 cell differentiation by IL-1 signaling (2009, background): “INTRODUCTION Th17 cells are a unique lineage of T cells that have been shown to be important in autoimmunity and clearance of mucosal infection by producing proinflammatory cytokines IL-17, IL-17F, and IL-22 (Dong, 2008; Ouyang et al., 2008).”