Oxidative Stress and Redox Modulation Potential in Type 1 Diabetes

Figure 1

Role of redox in the immunopathology of type 1 diabetes. An initial genetic or environmental insult to the beta cell triggers the release of beta cell antigens as well as the production of ROS. Beta cell antigens are phagocytosed, and ROS are able to stimulate redox-dependent transcription factors such as NF-κB, which leads to APC activation and cytokine secretion. ROS and proinflammatory cytokines secreted by APCs act as the third signal within the T-cell-APC immunological synapse, which occurs in the pancreatic lymph node. ROS play a critical role in the progression of naïve TH0 cells to cytokine-secreting TH1 cells. Release of IFNγ by TH1 cells then works directly on the beta cells as well as activates more APCs and CD8 cells, all of which can impart deleterious effects on the islets.