Type 1 diabetes (T1D) is an organ-specific autoimmune disease that results in the selective loss of pancreatic beta cells and an eventual deficit in insulin production to maintain glucose homeostasis. It is now increasingly accepted that this dynamic disease process is multifactorial; involves a variety of immune cells which contribute ...
Type 1 diabetes (T1D) is an organ-specific autoimmune disease that results in the selective loss of pancreatic beta cells and an eventual deficit in insulin production to maintain glucose homeostasis. It is now increasingly accepted that this dynamic disease process is multifactorial; involves a variety of immune cells which contribute to an inflamed pancreatic microenvironment; and that the condition is heterogenous, resulting in variable rates of subsequent beta cell damage. In this review, we will explore the current understanding of the cellular interactions between both resident and infiltrating immune cells within the pancreatic environment, highlighting key mechanisms which may promote the beta cell destruction and islet damage associated with T1D.
