ABSTRACT
Until 40 or so years ago, diabetes was regarded as a single disorder. Himsworth had commented in the 1930s on the insulin-resistant individual who required larger doses of insulin, but the designations of adult onset and juvenile onset were descriptive and unrelated to any perceived differences in mechanism. In the mid-1960s, the Belgian histopathologist, Willy Gepts, first described infiltration of lymphocytes in the islets of children who died within a few days of developing diabetes (1). He noted similarities to struma lymphomatosa of the thyroid, first described by Hashimoto in 1912, but regarded by the late 1950s as ‘‘autoimmune’’ because of the thyroid antibodies found in the serum of such patients. In 1974, Jorn Nerup described an association between childhood diabetes and the immune response or HLA genes on the short arm of chromosome 6 (2) and in the same year Franco Bottazzo and Deborah Doniach famously reported the presence of antibodies to the islet cells in blood samples from people with insulin-dependent diabetes (3).
