Type 1 diabetes mellitus is a T-cell-mediated autoimmune disease that results in the destruction of the insulin-producing β cells in the pancreatic islets of Langerhans. In spite of extensive genetic and immunological studies, mainly performed in the non-obese diabetic (NOD) spontaneous mouse model, the etiology of the autoimmune attack remains unknown. Several autoantigens have been identified and numerous studies have suggested a role for defective regulation of immune function. However, this account does not explain why the autoimmune process specifically affects the insulin-producing β cells. Thus, abnormal immune regulation might explain the predisposition to autoimmunity in general, but additional factors should then determine the target of the autoimmune attack. Here, we review the evidence that abnormalities in islet cell differentiation and function exist that might trigger the immune system towards β-cell autoimmunity in humans and NOD mice.

doi.org/10.1016/S1043-2760(02)00600-8, hdl.handle.net/1765/56980
Trends in Endocrinology and Metabolism
Department of Immunology

Rosmalen, J., Leenen, P., Pelegri, C., Drexhage, H., & Homo-Delarche, F. (2002). Islet abnormalities in the pathogenesis of autoimmune diabetes. Trends in Endocrinology and Metabolism (Vol. 13, pp. 209–214). doi:10.1016/S1043-2760(02)00600-8