Role of Increased ROS Dissipation in Prevention of T1D Lessons from the ALR Mouse

被引：30

作者：

Chen, Jing ^{[1
]}

Gusdon, Aaron M. ^{[1
]}

Thayer, Terri C. ^{[1
]}

Mathews, Clayton E. ^{[1
]}

机构：

[1] Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL 32610 USA

来源：

IMMUNOLOGY OF DIABETES V: FROM BENCH TO BEDSIDE | 2008年 / 1150卷

基金：

美国国家卫生研究院;

关键词：

type; 1; diabetes; reactive oxygen species; mitochondria; mouse model; genetics;

D O I：

10.1196/annals.1447.045

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Protection of pancreatic beta cells is an approach to prevent autoimmune type 1 diabetes (T1D) and to protect transplanted islets. Reactive oxygen species (ROS) are important mediators of beta cell death during the development of T1D. We have examined the role of elevated ROS dissipation in the prevention of T1D using the ALR mouse strain. The selection of ALR, for resistance against alloxan-induced free radical-mediated diabetes, led to a strain of mice with an elevated systemic as well as pancreatic ROS dissipation. Independent genetic mapping studies have identified ALR-derived diabetes protective loci. Conplastic and congenic mouse as well as cell line studies have confirmed the genetic mapping and demonstrated that the elevated ROS dissipation protects ALR beta cells from autoimmune destruction. Our data support the hypothesis that elevated ROS dissipation protects beta cells against autoimmune destruction and prevents T1D development.

引用

页码：157 / 166

页数：10

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