Document Detail


MicroRNA in TLR signaling and endotoxin tolerance.
MedLine Citation:
PMID:  21822296     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Toll-like receptors (TLRs) in innate immune cells are the prime cellular sensors for microbial components. TLR activation leads to the production of proinflammatory mediators and thus TLR signaling must be properly regulated by various mechanisms to maintain homeostasis. TLR4-ligand lipopolysaccharide (LPS)-induced tolerance or cross-tolerance is one such mechanism, and it plays an important role in innate immunity. Tolerance is established and sustained by the activity of the microRNA miR-146a, which is known to target key elements of the myeloid differentiation factor 88 (MyD88) signaling pathway, including IL-1 receptor-associated kinase (IRAK1), IRAK2 and tumor-necrosis factor (TNF) receptor-associated factor 6 (TRAF6). In this review, we comprehensively examine the TLR signaling involved in innate immunity, with special focus on LPS-induced tolerance. The function of TLR ligand-induced microRNAs, including miR-146a, miR-155 and miR-132, in regulating inflammatory mediators, and their impact on the immune system and human diseases, are discussed. Modulation of these microRNAs may affect TLR pathway activation and help to develop therapeutics against inflammatory diseases.
Authors:
Md A Nahid; Minoru Satoh; Edward Kl Chan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-08-08
Journal Detail:
Title:  Cellular & molecular immunology     Volume:  8     ISSN:  2042-0226     ISO Abbreviation:  Cell. Mol. Immunol.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-05     Completed Date:  2012-01-10     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  101242872     Medline TA:  Cell Mol Immunol     Country:  China    
Other Details:
Languages:  eng     Pagination:  388-403     Citation Subset:  IM    
Affiliation:
Department of Oral Biology, University of Florida, Gainesville, FL, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bacteria / growth & development
Bacterial Infections / immunology,  microbiology
Cytokines / genetics,  immunology,  metabolism
Endotoxins / immunology,  pharmacology*
Gene Expression Regulation / immunology*
Humans
Immune System Diseases / genetics
Immune Tolerance / genetics*
Immunity, Innate*
Interleukin-1 Receptor-Associated Kinases / genetics,  immunology,  metabolism
Mice
MicroRNAs / genetics,  immunology*,  metabolism
Myeloid Differentiation Factor 88 / genetics,  immunology,  metabolism
Rats
Signal Transduction / genetics,  immunology*
TNF Receptor-Associated Factor 6 / genetics,  immunology,  metabolism
Toll-Like Receptor 4 / genetics,  immunology,  metabolism
Grant Support
ID/Acronym/Agency:
AI47859/AI/NIAID NIH HHS; R01 AI047859/AI/NIAID NIH HHS; T32 AR007603/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Endotoxins; 0/MIRN132 microRNA, human; 0/MIRN146 microRNA, human; 0/MIRN155 microRNA, human; 0/MicroRNAs; 0/Myeloid Differentiation Factor 88; 0/TNF Receptor-Associated Factor 6; 0/Toll-Like Receptor 4; EC 2.7.11.1/Interleukin-1 Receptor-Associated Kinases
Comments/Corrections

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


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