Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance

• Published in: Biochimica et biophysica acta Vol. 1842; no. 3; pp. 446 - 462
• Main Authors: Lee, Byung-Cheol, Lee, Jongsoon
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.03.2014
• Subjects: Adipose tissue; Adipose Tissue - immunology; Adipose Tissue - metabolism; Adipose Tissue - pathology; Adipose tissue immune cell; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - metabolism; CD8-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - metabolism; Humans; Inflammation - immunology; Inflammation - metabolism; Inflammation - pathology; Insulin resistance; Insulin Resistance - genetics; Insulin Resistance - immunology; Macrophages - cytology; Macrophages - immunology; Neutrophils - immunology; Neutrophils - metabolism; Obesity - immunology; Obesity - metabolism; Obesity - pathology; Obesity-induced Inflammation; Th1 Cells - immunology; Th1 Cells - metabolism; FFA; Adipose tissue; RANTES; HFD; MHC; HMGB1; Obesity-induced Inflammation; MPO; TNF; CXCL5; TZDs; PPAR; CCR2; ABCA; AIM; T2D; IR; PKC; MAPK; PBMC; AT; GPR120; CLSs; NKT; NE; ROS; TCRs; Sorbs1; IKKb; dsDNA; CX3CR1; SVC; MCP-1; PRRs; CTLs; BLT; BM; IRS; NFkB; DAMPs; GFP; ASC; SOCS1; NLS; TAMs; CCL5; CXCR2; MGL1; TLR; RAGs; Treg; BMT; FABP; Nlrp3; Casp1; KLF4; ECM; JNKs; APC; Bregs; Insulin resistance; ATM; GLUT4; Adipose tissue immune cell; DC; thiazolidinediones; Sorbin and SH3 domain-containing protein 1; double stranded DNA; high fat diet; Caspase 1; nuclear factor kappa-light-chain-enhancer of activated B cells; macrophage galactose-type lectin 1; leukotriene B4 receptor; regulator T cells; green fluorescent protein; Insulin receptor substrate; Suppressor of cytokine signaling 1; Major histocompatibility complex; neutrophil elastase; Reactive oxygen species; bone marrow transplantation; mitogen-activated protein kinase; Tumor necrosis factors; ATP-binding cassette transporter; Dendritic cells; NOD-like receptor family, pyrin domain containing 3; bone marrow; Free fatty acids; apoptotic speck protein containing a caspase recruitment domain; AT macrophage; Regulated on Activation Normal T cell Expressed and Secreted; C-X-C motif receptor 2; extracellular matrix; Jun N-terminal kinases; G-protein coupled receptor 120; Protein kinase C; Krueppel-like factor 4; Glucose transporter type 4; tumor-associated macrophages; monocyte chemotactic protein-1; fatty-acid-binding protein; cytotoxic T cells; T cell receptors; high-mobility group box 1; Damage-associated molecular pattern molecules; Chemokine (C-C motif) ligand 5; C-C chemokine receptor type 2; CX3C chemokine receptor 1; antigen-presenting cell; peroxisome proliferator-activated receptors; Type 2 Diabetes; Pattern recognition receptors; Toll-like receptors; Recombination activating genes; C-X-C motif chemokine 5; stromal vascular cell; Natural Killer T cell; myeloperoxidase; Apoptosis inhibitor of macrophage; nuclear localization sequence; inhibitor of κB kinase-β; regulatory B cells; crown-like structures; insulin receptor; peripheral blood mononuclear cell
• ISSN: 0925-4439; 0006-3002; 1879-260X; 1878-2434
• DOI: 10.1016/j.bbadis.2013.05.017

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. •We discuss obesity-induced adipose tissue inflammation.•We discuss the cellular and molecular players of obesity-induced inflammation.•We discuss obesity-induced inflammation in the context of classical immunity.