Pancreatic islet inflammation: an emerging role for chemokines

被引:47
|
作者
Collier, J. Jason [1 ,2 ]
Sparer, Tim E. [3 ]
Karlstad, Michael D. [2 ]
Burke, Susan J. [4 ]
机构
[1] Pennington Biomed Res Ctr, Lab Islet Biol & Inflammat, 6400 Perkins Rd, Baton Rouge, LA 70808 USA
[2] Univ Tennessee, Hlth Sci Ctr, Grad Sch Med, Dept Surg, Knoxville, TN 37996 USA
[3] Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA
[4] Pennington Biomed Res Ctr, Lab Immunogenet, 6400 Perkins Rd, Baton Rouge, LA 70808 USA
关键词
cytokine; chemokine; diabetes; islet; inflammation; NF-KAPPA-B; BETA-CELL FUNCTION; TYPE-1; DIABETES-MELLITUS; NECROSIS-FACTOR-ALPHA; SATURATED FATTY-ACID; INSULIN-RESISTANCE; SIGNAL-TRANSDUCTION; INTERFERON-GAMMA; BIASED AGONISM; NITRIC-OXIDE;
D O I
10.1530/JME-17-0042
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Both type 1 and type 2 diabetes exhibit features of inflammation associated with alterations in pancreatic islet function and mass. These immunological disruptions, if unresolved, contribute to the overall pathogenesis of disease onset. This review presents the emerging role of pancreatic islet chemokine production as a critical factor regulating immune cell entry into pancreatic tissue as well as an important facilitator of changes in tissue resident leukocyte activity. Signaling through two specific chemokine receptors (i.e., CXCR2 and CXCR3) is presented to illustrate key points regarding ligand-mediated regulation of innate and adaptive immune cell responses. The prospective roles of chemokine ligands and their corresponding chemokine receptors to influence the onset and progression of autoimmune-and obesity-associated forms of diabetes are discussed.
引用
收藏
页码:R33 / R46
页数:14
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