Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8260431 | Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease | 2014 | 17 Pages |
Abstract
There is increasing evidence showing that inflammation is an important pathogenic mediator of the development of obesity-induced insulin resistance. It is now generally accepted that tissue-resident immune cells play a major role in the regulation of this obesity-induced inflammation. The roles that adipose tissue (AT)-resident immune cells play have been particularly extensively studied. AT contains most types of immune cells and obesity increases their numbers and activation levels, particularly in AT macrophages (ATMs). Other pro-inflammatory cells found in AT include neutrophils, Th1 CD4 T cells, CD8 T cells, B cells, DCs, and mast cells. However, AT also contains anti-inflammatory cells that counter the pro-inflammatory immune cells that are responsible for the obesity-induced inflammation in this tissue. These anti-inflammatory cells include regulatory CD4 T cells (Tregs), Th2 CD4 T cells, and eosinophils. Hence, AT inflammation is shaped by the regulation of pro- and anti-inflammatory immune cell homeostasis, and obesity skews this balance towards a more pro-inflammatory status. Recent genetic studies revealed several molecules that participate in the development of obesity-induced inflammation and insulin resistance. In this review, the cellular and molecular players that participate in the regulation of obesity-induced inflammation and insulin resistance are discussed, with particular attention being placed on the roles of the cellular players in these pathogeneses. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease.
Keywords
ECMKLF4PBMCDAMPsdsDNAASCGFPFFAHFDMCP-1PPARIRSAPCTLRT2DPKCCcl5HMGB1CX3CR1NLSGLUT4BLTBMTCCR2C-C chemokine receptor type 2TregSVCSOCS1CX3C chemokine receptor 1GPR120CXCR2CXCL5NLRP3PRRsNFkBNKTFABPCASP1CLSSABCAIkkBJNKsTAMsG-protein coupled receptor 120Jun N-terminal kinasesRegulated on activation normal T cell expressed and secretedTNFNod-like receptor family, pyrin domain containing 3RAGsCTLsMPOdouble stranded DNAMAPKROSTCRsTZDsantigen-presenting cellFree fatty acidsneutrophil elastaseinsulin receptor substrateAdipose tissueBregsthiazolidinedioneshigh-mobility group box 1ATP-binding cassette transporterATMnuclear localization sequenceType 2 diabetesHigh fat dietCrown-like structuressuppressor of cytokine signaling 1natural killer T cellPeripheral blood mononuclear cellcytotoxic T cellsregulatory B cellsDendritic cellsTumor necrosis factorsnuclear factor kappa-light-chain-enhancer of activated B cellsExtracellular matrixTumor-associated macrophagesMHCmajor histocompatibility complexRANTESbone marrowInsulin resistancedamage-associated molecular pattern moleculesmyeloperoxidaseGlucose transporter type 4AIMMonocyte chemotactic protein-1green fluorescent proteinFatty-acid-binding proteinProtein kinase Cmitogen-activated protein kinaseBone marrow transplantationRecombination activating genescaspase 1chemokine (C-C motif) ligand 5Reactive oxygen speciesleukotriene B4 receptorinsulin receptorPeroxisome proliferator-activated receptorsT cell receptorspattern recognition receptorsToll-like receptors
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Authors
Byung-Cheol Lee, Jongsoon Lee,