期刊
IMMUNOLOGY OF DIABETES V: FROM BENCH TO BEDSIDE
卷 1150, 期 -, 页码 157-166出版社
WILEY-BLACKWELL
DOI: 10.1196/annals.1447.045
关键词
type 1 diabetes; reactive oxygen species; mitochondria; mouse model; genetics
资金
- Juvenile Diabetes Research Foundation
- National Institutes of Health [AT56374, DK74656]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI056374] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R56DK074656, R01DK074656] Funding Source: NIH RePORTER
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.
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