Journal
IMMUNITY
Volume 34, Issue 4, Pages 566-578Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.03.018
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Funding
- DFG
- Sonderfor-schungsbereich [621]
- Project A2
- European Union [MUGEN LSHG-CT-2005-005203]
- National Institutes of Health [GM07739]
- Cancer Research Institute
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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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