Document Detail


Lipopolysaccharide-mediated IL-10 transcriptional regulation requires sequential induction of type I IFNs and IL-27 in macrophages.
MedLine Citation:
PMID:  21041726     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
IL-10 is a potent anti-inflammatory molecule that regulates excessive production of inflammatory cytokines during an infection or tissue damage. Dysregulation of IL-10 is associated with a number of autoimmune diseases, and so, understanding the mechanisms by which IL-10 gene expression is regulated remains an important area of study. Macrophages represent a major source of IL-10, which is generated in response to TLR signaling as a feedback mechanism to curtail inflammatory response. In this study, we identify a signaling pathway in murine bone marrow-derived macrophages in which activation of TLR4 by LPS induces the expression of IL-10 through the sequential induction of type I IFNs followed by induction and signaling through IL-27. We demonstrate that IL-27 signaling is required for robust IL-10 induction by LPS and type I IFNs. IL-27 leads directly to transcription of IL-10 through the activation of two required transcription factors, STAT1 and STAT3, which are recruited to the IL-10 promoter. Finally, through systematic functional promoter-reporter analysis, we identify three cis elements within the proximal IL-10 promoter that play an important role in regulating transcription of IL-10 in response to IL-27.
Authors:
Shankar Subramanian Iyer; Amir Ali Ghaffari; Genhong Cheng
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Publication Detail:
Type:  Journal Article     Date:  2010-11-01
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-18     Completed Date:  2011-01-10     Revised Date:  2011-03-17    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6599-607     Citation Subset:  AIM; IM    
Affiliation:
Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autocrine Communication / genetics,  immunology
Bone Marrow Cells / immunology,  metabolism
Cell Line
Interferon Type I / biosynthesis*,  genetics
Interleukin-10 / genetics*,  metabolism
Interleukins / biosynthesis*,  genetics,  physiology
Lipopolysaccharides / pharmacology*
Macrophages / immunology*,  metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Paracrine Communication / genetics,  immunology
Promoter Regions, Genetic / immunology*
Signal Transduction / genetics,  immunology
Transcription, Genetic / immunology*
Transcriptional Activation / immunology*
Grant Support
ID/Acronym/Agency:
R01 AI056154-07/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Il27 protein, mouse; 0/Interferon Type I; 0/Interleukins; 0/Lipopolysaccharides; 130068-27-8/Interleukin-10

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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