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We are analyzing https://www.nature.com/articles/ni.1613.

Title:
A critical function for transforming growth factor-β, interleukin 23 and proinflammatory cytokines in driving and modulating human TH-17 responses | Nature Immunology
Description:
Interleukin 17 (IL-17)–producing T helper 17 cells (TH-17 cells) have been described as a T helper cell subset distinct from T helper type 1 (TH1) and TH2 cells, with specific functions in antimicrobial defense and autoimmunity. The factors driving human TH-17 differentiation remain controversial. Using a systematic approach combining experimental and computational methods, we show here that transforming growth factor-β, interleukin 23 (IL-23) and proinflammatory cytokines (IL-1β and IL-6) were all essential for human TH-17 differentiation. However, individual TH-17 cell–derived cytokines, such as IL-17, IL-21, IL-22 and IL-6, as well as the global TH-17 cytokine profile, were differentially modulated by TH-17-promoting cytokines. Transforming growth factor-β was critical, and its absence induced a shift from a TH-17 profile to a TH1-like profile. Our results shed new light on the regulation of human TH-17 differentiation and provide a framework for the global analysis of T helper responses.
Website Age:
30 years and 10 months (reg. 1994-08-11).

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  • Science
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Custom-built

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Keywords {🔍}

pubmed, article, cas, google, scholar, cells, immunol, nature, interleukin, nat, central, helper, cell, differentiation, human, transforming, growth, access, factorβ, med, content, analysis, exp, cytokines, responses, inflammation, cookies, distinct, rev, paris, france, privacy, essential, data, immunology, critical, proinflammatory, nicolas, servant, philippe, hupé, type, computational, cytokine, tgfβ, autoimmune, development, immunity, producing, receptor,

Topics {✒️}

nature portfolio permissions reprints tissue research privacy policy advertising transforming growth factor-β social media author information authors nature 441 nature 448 nature th17 cell-derived tgf-β1 laboratoire d'immunologie clinique inhibit ifn-γ expression author correspondence quantitative rt-pcr analysis philippe hup� computational data analysis nuclear receptor rorγt springerlink instant access permissions personal data de waal malefyt data protection receptor-activated monocytes induces autoimmune inflammation require tgf-β privacy cell receptor ligation 17 cell–mediated pathology european economic area o'garra joint autoimmune inflammation 17 cell–derived cytokines reduced th17 responses cooperatively enhance expression vassili soumelis article volpe cell-mediated colitis institutional subscriptions read lymphokine secretion lead card9-dependent coupling stat3-dependent manner mycobacterium tuberculosis challenge bone regeneration disorder th17 cell differentiation helper cell subsets th17 cells contribute accepting optional cookies autoimmune encephalomyelitis

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Schema {🗺️}

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      name:Institut National de la Santé et de la Recherche Médicale U653, Paris, France
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