Differentiation and function of Th17 T cells.

By Brigitta Stockinger, M. Veldhoen. Current Opinion in Immunology, 2007

812 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f78cf740660c746008e208c803f4180e2379c9d4

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Citations in the corpus

Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “In addition to previously recognized T helper 1 (Th1) and Th2 fates, naive CD4 T cells can also differentiate into Th17 and regulatory T (Treg) cells; the balance of Th17 and Treg cells is now considered to be critical for host immunity and the preservation of tolerance (Bettelli et al., 2008; Stock”
The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, positive): “It is believed that Th17 lymphocytes, which secrete interleukin-17, may play an important role in neuronal killing (Stockinger and Veldhoen, 2007).”
Microbial flora drives interleukin 22 production in intestinal NKp46+ cells that provide innate mucosal immune defense. (2008, background): “the soluble factors IL-6, IL-21, IL-23, and TGF-b and activates STAT3 to induce RORgt expression (Chen and O’Shea, 2008; Stockinger and Veldhoen, 2007; Weaveret al., 2007).”
The differentiation of human TH-17 cells requires transforming growth factor-β and induction of the nuclear receptor RORγt (2008, background): “1610" language="eng" relation="no"> T H -17 cells, T helper cells that produce interleukin 17 (IL-17) and other proinflammatory cytokines, have been shown to have key functions in several mouse autoimmune disease models and are thought to be similarly involved in human diseas”
Late Developmental Plasticity in the T Helper 17 Lineage (2009, positive): “T helper 17 is a third major CD4+ T cell effector subset important in host protection and autoinflammatory disorders (McGeachy and Cua, 2008; Stockinger and Veldhoen, 2007; Weaver et al., 2007).”
Specific microbiota direct the differentiation of Th17 cells in the mucosa of the small intestine (2008, positive): “There has been extensive investigation of the cytokine requirements and genetic regulation in Th17 cell differentiation both under well-defined conditions in vitro and in the context of inflammatory stimuli in vivo (Bettelli et al., 2007; Ivanov et al., 2007; Stockinger and Veldhoen, 2007).”
The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities (2012, background): “In particular, CD4 + T cells become polarized during activation into Th1, Th2, Th17, Treg, or other T helper subtypes (180, 213, 242).”
Inflammatory signals in dendritic cell activation and the induction of adaptive immunity (2009, background): “Reis e Sousa, unpublished data) and IL-23 (46), which are, respectively, required to drive the differentiation and promote the survival of that type of effector T cell (84, 85).”
IL‐23 and the Th17 pathway promote inflammation and impair antifungal immune resistance (2007, background): “IL-23, although not involved in Th17 differentiation, plays an important role in maintaining Th17 effector function [3, 4 ]. Th17 cells are responsible for various organ-related autoimmune diseases [5, 6], and both IL-23 and the Th17 pathway correlate with disease severity and immunopathology in di”
Review of ustekinumab, an interleukin-12 and interleukin-23 inhibitor used for the treatment of plaque psoriasis (2010, positive): “IL-23 stimulates survival and proliferation of Th17 cells, a key cell that regulates the production of other inflammatory cytokines (IL-17, IL-22, IL-21, IL-6, tumor necrosis factor (TNF)-α) and is overproduced in dendritic cells and keratinocytes found psoriatic plaques.(8,9) Th1 cells develop from”