Pathogenesis of type 1 diabetes: lessons from natural history studies of high-risk individuals
Article first published online: 29 JAN 2013
© 2013 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1281, The Year in Diabetes and Obesity pages 1–15, April 2013
How to Cite
Nokoff, N. and Rewers, M. (2013), Pathogenesis of type 1 diabetes: lessons from natural history studies of high-risk individuals. Annals of the New York Academy of Sciences, 1281: 1–15. doi: 10.1111/nyas.12021
- Issue published online: 1 APR 2013
- Article first published online: 29 JAN 2013
- type 1 diabetes;
- beta cell;
- islet autoantibody
Type 1 diabetes (T1D) is an autoimmune disease characterized by known genetic risk factors with T cell–mediated infiltration and destruction of the beta cells within pancreatic islets. Autoantibodies are the most significant preclinical marker of T1D, and birth cohort studies have provided important insights into the natural history of autoimmunity and T1D. While HLA remains the strongest genetic risk factor, a number of novel gene variants associated with T1D have been found through genome-wide studies, some of which have been linked to suspected environmental risk factors. Multiple environmental factors that have been suggested to play a role in the development of T1D await confirmation. Current risk-stratification models for T1D take into account genetic risk factors and autoantibodies. In the future, metabolic profiles, epigenetics, as well as environmental risk factors may be included in such models.