Type 2 diabetes as an inflammatory disease

被引：2823

作者：

Donath, Marc Y. ^{[1
]}

Shoelson, Steven E. ^{[2
]}

机构：

[1] Univ Basel Hosp, Clin Endocrinol Diabet & Metab, CH-4031 Basel, Switzerland

[2] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA

来源：

NATURE REVIEWS IMMUNOLOGY | 2011年 / 11卷 / 02期

关键词：

NECROSIS-FACTOR-ALPHA; MONOCYTE CHEMOATTRACTANT PROTEIN-1; ENDOPLASMIC-RETICULUM STRESS; PANCREATIC BETA-CELL; REGULATORY T-CELLS; ACTIVATED SIGNALING PATHWAYS; MONOUNSATURATED FATTY-ACIDS; ADIPOSE-TISSUE MACROPHAGES; IL-1 RECEPTOR ANTAGONIST; DIET-INDUCED OBESITY;

D O I：

10.1038/nri2925

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Components of the immune system are altered in obesity and type 2 diabetes (T2D), with the most apparent changes occurring in adipose tissue, the liver, pancreatic islets, the vasculature and circulating leukocytes. These immunological changes include altered levels of specific cytokines and chemokines, changes in the number and activation state of various leukocyte populations and increased apoptosis and tissue fibrosis. Together, these changes suggest that inflammation participates in the pathogenesis of T2D. Preliminary results from clinical trials with salicylates and interleukin-1 antagonists support this notion and have opened the door for immunomodulatory strategies for the treatment of T2D that simultaneously lower blood glucose levels and potentially reduce the severity and prevalence of the associated complications of this disease.

引用

页码：98 / 107

页数：10

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