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    block this user Werner Muller

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    Faculty of Life Science, University of Manchester, Manchester

    Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation.

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    Effector CD4+ T cell subsets, whose differentiation is facilitated by distinct cytokine cues, amplify the corresponding type of inflammatory response. Regulatory T (Treg) cells integrate environmental cues to suppress particular types of inflammation. In this regard, STAT3, a transcription factor essential for T helper 17 (Th17) cell differentiation, is necessary for Treg cell-mediated control of Th17 cell responses. Here, we showed that anti-inflammatory interleukin-10 (IL-10), and not proinflammatory IL-6 and IL-23 cytokine signaling, endowed Treg cells with the ability to suppress pathogenic Th17 cell responses. Ablation of the IL-10 receptor in Treg cells resulted in selective dysregulation of Th17 cell responses and colitis similar to that observed in mice harboring STAT3-deficient Treg cells. Thus, Treg cells limit Th17 cell inflammation by serving as principal amplifiers of negative regulatory circuits operating in immune effector cells.

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    Description

    Title : Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation.
    Author(s) : Ashutosh Chaudhry, Robert M Samstein, Piper Treuting, Yuqiong Liang, Marina C Pils, Jan-Michael Heinrich, Robert S Jack, F Thomas Wunderlich, Jens C Brüning, Werner Müller, Alexander Y Rudensky
    Abstract : Effector CD4+ T cell subsets, whose differentiation is facilitated by distinct cytokine cues, amplify the corresponding type of inflammatory response. Regulatory T (Treg) cells integrate environmental cues to suppress particular types of inflammation. In this regard, STAT3, a transcription factor essential for T helper 17 (Th17) cell differentiation, is necessary for Treg cell-mediated control of Th17 cell responses. Here, we showed that anti-inflammatory interleukin-10 (IL-10), and not proinflammatory IL-6 and IL-23 cytokine signaling, endowed Treg cells with the ability to suppress pathogenic Th17 cell responses. Ablation of the IL-10 receptor in Treg cells resulted in selective dysregulation of Th17 cell responses and colitis similar to that observed in mice harboring STAT3-deficient Treg cells. Thus, Treg cells limit Th17 cell inflammation by serving as principal amplifiers of negative regulatory circuits operating in immune effector cells.
    Subject : unspecified
    Area : Other
    Language : English
    Year : 2011

    Affiliations Faculty of Life Science, University of Manchester, Manchester
    Journal : Immunity
    Volume : 34
    Issue : 4
    Pages : 566-578
    Url : http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3088485&tool=pmcentrez&rendertype=abstract

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    Werner's Peer Evaluation activity

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