TY - JOUR
T1 - Interleukin-10 Signaling in Regulatory T Cells Is Required for Suppression of Th17 Cell-Mediated Inflammation
AU - Chaudhry, Ashutosh
AU - Samstein, Robert M.
AU - Treuting, Piper
AU - Liang, Yuqiong
AU - Pils, Marina C.
AU - Heinrich, Jan Michael
AU - Jack, Robert S.
AU - Wunderlich, F. Thomas
AU - Brüning, Jens C.
AU - Müller, Werner
AU - Rudensky, Alexander Y.
N1 - GM07739, NIGMS NIH HHS, United StatesR37 AI034206-19, NIAID NIH HHS, United States, Howard Hughes Medical Institute, United States
PY - 2011/4/22
Y1 - 2011/4/22
N2 - 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. © 2011 Elsevier Inc.
AB - 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. © 2011 Elsevier Inc.
U2 - 10.1016/j.immuni.2011.03.018
DO - 10.1016/j.immuni.2011.03.018
M3 - Article
C2 - 21511185
SN - 1074-7613
VL - 34
SP - 566
EP - 578
JO - Immunity
JF - Immunity
IS - 4
ER -