Immune and Pancreatic β Cell Interactions in Type 1 Diabetes. (December 2016)

• Record Type: Journal Article
• Authors: Boldison, Joanne; Wong, F. Susan
• Is Part Of: Trends in endocrinology and metabolism. Volume 27:Number 12(2016)
• Page Start: 856
• Page End: 867
• Publication Date: 2016-12
• Subjects: immune crosstalk -- pancreatic islets -- inflammation -- type 1 diabetes -- autoimmune disease; Endocrinology -- Periodicals; Metabolism -- Periodicals; Metabolism; 616.4
• DOI: 10.1016/j.tem.2016.08.007
• Languages: English
• ISSNs: 1043-2760

Abstract

Abstract : The autoimmune destruction of the pancreatic islet β cells is due to a targeted lymphocyte attack. Different T cell subsets communicate with each other and with the insulin-producing β cells in this process, with evidence not only of damage to the tissue cells but also of lymphocyte regulation. Here we explore the various components of the immune response as well as the cellular interactions that are involved in causing or reducing immune damage to the β cells. We consider these in the light of the possibility that understanding them may help us identify therapeutic targets to reduce the damage and destruction leading to type 1 diabetes. Trends: In type 1 diabetes (T1D), β cells are highly sensitive to selective damage and recruit immune cells by chemokine production. These immune cells directly damage β cells and induce enzymes and cytokines that cause free radical- and cytokine-induced apoptosis. Damaged islets express innate immune receptors, engagement of which may amplify β cell destruction contributing to their own destruction. Interestingly, damaged and functional islets coexist. Immune regulatory cells and regulatory mechanisms induced by islet cells counterbalance inflammation. Communication between immune cells and resident islet β cells during inflammation is dependent on the pancreatic microenvironment. Therapeutically targeting the direct and indirect mediators of β cell damage to prevent further destruction combined with boosting β cell numbers and function are important joint targets in developing therapies for T1D.