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

By A. Chaudhry, Robert Samstein, P. Treuting, Yuqiong Liang, Marina C. Pils, J. Heinrich, R. Jack, F. Wunderlich, Jens C. Brüning, Werner Müller and 1 more. Immunity, 2011

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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 pro-inflammatory 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.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/3a10823e73ce30fed5220a408b3125ece38df28d

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In Immunology

Citations in the corpus

The Microbiome in Infectious Disease and Inflammation (2012, positive): “Deficiency of Stat3 or IL-10R in Treg cells selectively interferes with their capacity to suppress Th17 cell responses (234, 235).”