Document Detail


Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation.
MedLine Citation:
PMID:  21511185     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Ashutosh Chaudhry; Robert M Samstein; Piper Treuting; Yuqiong Liang; Marina C Pils; Jan-Michael Heinrich; Robert S Jack; F Thomas Wunderlich; Jens C Brüning; Werner Müller; Alexander Y Rudensky
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Immunity     Volume:  34     ISSN:  1097-4180     ISO Abbreviation:  Immunity     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-22     Completed Date:  2011-06-17     Revised Date:  2013-03-26    
Medline Journal Info:
Nlm Unique ID:  9432918     Medline TA:  Immunity     Country:  United States    
Other Details:
Languages:  eng     Pagination:  566-78     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Howard Hughes Medical Institute and Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Lineage
Colitis / immunology*,  pathology
Interleukin-10 / immunology*,  metabolism
Mice
Mice, Knockout
Phosphorylation
Receptors, Interleukin-10 / deficiency,  immunology
STAT3 Transcription Factor / immunology,  metabolism
Signal Transduction*
T-Lymphocytes, Regulatory / cytology,  immunology*
Th17 Cells / immunology*
Grant Support
ID/Acronym/Agency:
F30 DK091968/DK/NIDDK NIH HHS; GM07739/GM/NIGMS NIH HHS; R37 AI034206-19/AI/NIAID NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/IL10 protein, mouse; 0/Receptors, Interleukin-10; 0/STAT3 Transcription Factor; 0/Stat3 protein, mouse; 130068-27-8/Interleukin-10
Comments/Corrections
Comment In:
Immunity. 2011 Apr 22;34(4):460-2   [PMID:  21511180 ]

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