Unknown

Dataset Information

0

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


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.

SUBMITTER: Chaudhry A 

PROVIDER: S-EPMC3088485 | BioStudies | 2011-01-01

REPOSITORIES: biostudies

Similar Datasets

2011-01-01 | S-EPMC3258585 | BioStudies
2008-01-01 | S-EPMC2630532 | BioStudies
2010-01-01 | S-EPMC3008772 | BioStudies
2017-01-01 | S-EPMC5716359 | BioStudies
2009-01-01 | S-EPMC2814877 | BioStudies
1000-01-01 | S-EPMC3012178 | BioStudies
2018-01-01 | S-EPMC6174281 | BioStudies
2011-01-01 | S-EPMC3133678 | BioStudies
1000-01-01 | S-EPMC3217413 | BioStudies
1000-01-01 | S-EPMC4618596 | BioStudies