Summary
Immunological mechanisms which precipitate autoimmune diabetes involve the influence of a genetic footprint on the phenotype of the T-cell response to self-antigens, and on development of pathological outcomes in immune responses resulting in T1D. For one of the human diabetes antigens, proinsulin, recent findings allow the emergence of a model in which elements of genetically biased T-cell development and peptide epitope-specific T-cell avidity result in expression of autoimmune disease. Understanding such self-reactive T-cell responses is key to implementation of specific immunotherapies for modulating disease risk and progression.