Higher molecular weight insulin precursors as autoantigens in type I diabetes

Hypothetically, the formation of abnormal insulin precursors due to genetic and/or acquired disorders would result in autoantigens by virtue of the altered tertiary structure. These are unlikely to be accessible to the converting enzymes which in turn should produce extended exposure to the immune system. Subsequent humoral and cell-mediated immune response might thus initiate or aggravate the autoimmune destruction of B-cells in subjects genetically susceptible to Type I diabetes.