期刊
FRONTIERS IN ENDOCRINOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fendo.2018.00175
关键词
redox signaling; reactive oxygen species; type 1 diabetes; islet transplantation; immune rejection; immunology; encapsulation
资金
- American Diabetes Association [7-12-CD-11]
- Juvenile Diabetes Research Foundation [1-SRA-2015-42-A-N]
- National Institutes of Health [DK099550, T32.GM109780]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM008111] Funding Source: NIH RePORTER
Type 1 diabetes is an autoimmune disease that results in the progressive destruction of insulin-producing pancreatic beta-cells inside the islets of Langerhans. The loss of this vital population leaves patients with a lifelong dependency on exogenous insulin and puts them at risk for life-threatening complications. One method being investigated to help restore insulin independence in these patients is islet cell transplantation. However, challenges associated with transplant rejection and islet viability have prevented long-term beta-cell function. Redox signaling and the production of reactive oxygen species (ROS) by recipient immune cells and transplanted islets themselves are key players in graft rejection. Therefore, dissipation of ROS generation is a viable intervention that can protect transplanted islets from immune-mediated destruction. Here, we will discuss the newly appreciated role of redox signaling and ROS synthesis during graft rejection as well as new strategies being tested for their efficacy in redox modulation during islet cell transplantation.
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