Review Article: Autoimmunity and Pathogenesis of Type 1 Diabetes

Abstract Type 1A diabetes mellitus results from autoimmune de-struction of the insulin-producing beta cells in the islets of Langerhans. This process occurs in genetically susceptible subjects, is probably triggered by one or more environmental agents, and usually progresses over many months or years during which the subject is asymptomatic and euglycemic. Thus, genetic markers for type 1A diabetes are present from birth, immune markers are detectable after the onset of the autoimmune process, and metabolic markers can be detected with sensitive tests once enough beta cell damage has occurred, but before the onset of symptomatic hyperglycemia. This long latent period is a reflection of the large number of functioning beta cells that must be lost before hyperglycemia occurs. Type 1B diabetes mellitus refers to nonautoimmune islet destruction (Type 1B diabetes). Both genetic and environmental factors contribute to the risk of developing type 1 diabetes mellitus (T1DM). In genet-ically susceptible individuals, exposure to one or more envi-ronmental agents appears to trigger an immune response that ultimately causes destruction of the insulin-producing pancre-atic beta cells. Identification of these factors should lead to a better understanding of the pathogenesis of the disease and aid in developing strategies to prevent T1DM. They include: - Viral infections, particularly enterovirus infections. - Immunizations. - Diet, especially exposure to cow's milk at an early age. - Higher socioeconomic status. - Obesity. - Vitamin D deficiency. - Perinatal factors such as maternal age, history of preeclamp-sia, and neonatal jaundice. Low birth weight decreases the risk of developing T1DM.