Chapter 19
Oxidative stress and type 1 diabetes
Chao Liu,
Clayton E. Mathews,
Jing Chen,
Chao Liu
Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL, USA
Search for more papers by this authorClayton E. Mathews
Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL, USA
Search for more papers by this authorJing Chen
Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL, USA
Search for more papers by this authorChao Liu,
Clayton E. Mathews,
Jing Chen,
Chao Liu
Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL, USA
Search for more papers by this authorClayton E. Mathews
Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL, USA
Search for more papers by this authorJing Chen
Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL, USA
Search for more papers by this authorBook Editor(s):Donald Armstrong,
Robert D. Stratton,
Donald Armstrong
Department of Biotechnical and Clinical Laboratory Sciences, State University of New York at Buffalo, Buffalo, NY, USA
Search for more papers by this authorRobert D. Stratton
Department of Ophthamology, University of Florida College of Medicine, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, US
Search for more papers by this authorSummary
This chapter reviews the role of free radicals during the pathogenesis of type 1 diabetes (T1D), both in the immune system and on the target β cells. Reactive oxygen species (ROS) contribute to β-cell dysfunction during the development of diabetes. Autoimmune β-cell destruction is a fundamental feature in the pathogenesis of T1D. β cells are considered to be particularly vulnerable to oxidative damage compared to other tissues as a result of lower antioxidant defenses. This exquisite sensitivity has been proposed to play a role in the pathogenesis of T1D. A preponderance of evidence suggesting that ROS participate β-cell death during T1D development has come from studies using mouse models. Phagocyte NADPH oxidase (NOX2) is critical for the production of ROS as biological messengers that participate in signal transduction within lymphocytes. NOX2 has been proposed to be critical to dendritic cell-mediated diabetogenic CD8+ T cell priming through cross-presentation.
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