Type 2 diabetes mellitus-an autoimmune disease?

被引:82
|
作者
Velloso, Licio A. [1 ]
Eizirik, Decio L. [2 ]
Cnop, Miriam [3 ]
机构
[1] Univ Estadual Campinas, DCM FCM UNICAMP, Lab Cell Signalling, Obes & Comorbid Res Ctr, BR-13084970 Sao Paulo, Brazil
[2] Univ Libre Bruxelles, Expt Med Lab, Fac Med, B-1070 Brussels, Belgium
[3] Univ Libre Bruxelles, Div Endocrinol, Erasmus Hosp, B-1070 Brussels, Belgium
关键词
ENDOPLASMIC-RETICULUM STRESS; ISLET-ASSOCIATED MACROPHAGES; DIET-INDUCED OBESITY; REGULATORY T-CELLS; INSULIN-RESISTANCE; ADIPOSE-TISSUE; GLUCOSE-HOMEOSTASIS; IMMUNE-RESPONSES; INFLAMMATION; AUTOANTIBODIES;
D O I
10.1038/nrendo.2013.131
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Inflammation-induced inhibition of the insulin signalling pathway can lead to insulin resistance and contribute to the development of type 2 diabetes mellitus (T2DM). Obesity and insulin resistance are associated with a chronic but subclinical inflammatory process that impairs insulin action in most tissues and could also hamper pancreatic 13-cell function. The involvement of monocytic cells and the profiles of the chemokines and cytokines induced by this inflammation suggest an innate immune response. However, emerging data indicate that elements of the adaptive immune system could also be involved. As activation of an adaptive response requires antigen specificity, some researchers have hypothesized that T2DM evolves from an innate immune response to an autoimmune condition. In this Perspectives article, we present the arguments for and against this hypothesis and discuss which mechanisms could be involved in a putative switch from innate immunity to autoimmunity.
引用
收藏
页码:750 / 755
页数:6
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