| First Author | Chaudhry A | Year | 2011 |
| Journal | Immunity | Volume | 34 |
| Issue | 4 | Pages | 566-78 |
| PubMed ID | 21511185 | Mgi Jnum | J:171597 |
| Mgi Id | MGI:4950615 | Doi | 10.1016/j.immuni.2011.03.018 |
| Citation | Chaudhry A, et al. (2011) Interleukin-10 signaling in regulatory T cells is required for suppression of th17 cell-mediated inflammation. Immunity 34(4):566-78 |
| abstractText | 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. |
