Endoplasmic reticulum stress in beta cells and autoimmune diabetes

被引：51

作者：

Clark, Amy L. ^{[1
]}

Urano, Fumihiko ^{[2
,3
]}

机构：

[1] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Med, Div Endocrinol Metab & Lipid Res, St Louis, MO 63110 USA

[3] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2016年 / 43卷

基金：

美国国家卫生研究院;

关键词：

THIOREDOXIN-INTERACTING PROTEIN; ANTI-CD3; MONOCLONAL-ANTIBODY; UP-REGULATED PROTEIN-1; ER STRESS; T-CELLS; CHROMOGRANIN-A; TYPE-1; APOPTOSIS; DEATH; CALCIUM;

D O I：

10.1016/j.coi.2016.09.006

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Type 1 diabetes results from the autoimmune destruction of pancreatic beta cells, leading to insulin deficiency and hyperglycemia. Although multiple attempts have been made to slow the autoimmune process using immunosuppressive or immunomodulatory agents, there are still no effective treatments that can delay or reverse the progression of type 1 diabetes in humans. Recent studies support endoplasmic reticulum (ER) as a novel target for preventing the initiation of the autoimmune reaction, propagation of inflammation, and beta cell death in type 1 diabetes. This review highlights recent findings on ER stress in beta cells and development of type 1 diabetes and introduces potential new treatments targeting the ER to combat this disorder.

引用

页码：60 / 66

页数：7

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