Autoantibodies in diabetes mellitus [Autoanticorpi nel diabete mellito]

Summary: Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease caused by the selective destruction of insulin-secreting pancreatic beta cells by a T-cell mediated inflammatory process. B-lymphocytes play a critical role as antigen-presenting cells and as precursors of plasma cells that produce islet autoantibodies. Islet autoantibodies originally identified in sera from patients with T1DM by the indirect immunofluorescence technique on criostatic sections of human pancreas are directed against several autoantigens, such as insulin, glutamic acid decarboxylase (GAD65), protein-tyrosin phosphatase IA-2 and zinc transporter T8 (ZnT8). These autoantibodies are not pathogenic, but they are useful clinical markers of the ongoing autoimmune process. When present in the serum of patients with diabetes mellitus they enable the discrimination between autoimmune and non autoimmune forms. More specifically, latent autoimmune diabetes in adults (LADA) is identified by the presence of GAD65 autoantibodies (GADA) in subjects with non-insulin-dependent diabetes, but with an increased risk for the future development of insulin-dependency. Furthermore, the presence of circulating islet autoantibodies enables the estimate of the risk for the future development of T1DM in normoglycemic individuals.