Islet autoimmunity in human type 1 diabetes: initiation and progression from the perspective of the beta cell

Type 1 diabetes results from the poorly understood process of islet autoimmunity, which ultimately leads to the loss of functional pancreatic beta cells. Mounting evidence supports the notion that the activation and evolution of islet autoimmunity in genetically susceptible people is contingent upon early life exposures affecting the islets, especially beta cells. Here, we review some of the recent advances and studies that highlight the roles of these changes as well as antigen presentation and stress response pathways in beta cells in the onset and propagation of the autoimmune process in type 1 diabetes. Future progress in this area holds promise for advancing islet- and beta cell-directed therapies that could be implemented in the early stages of the disease and could be combined with immunotherapies.

Automated summary

Type 1 diabetes occurs when the body's immune system mistakenly attacks and destroys pancreatic beta cells. This review highlights recent advances in understanding how early life exposures and stress response pathways impact beta cells and contribute to the autoimmune process in type 1 diabetes. Progress in this area holds promise for developing targeted therapies that could be implemented in the early stages of the disease, potentially in combination with immunotherapies.