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In the mid 1960s, the Belgian histopathologist Gepts [1] first described lymphocytes infiltrating the islets of children who died within a few days of developing diabetes. In 1974, Nerup et al. [2] found an association between childhood diabetes and the immune response or HLA genes on the short arm of chromosome 6. That same year, Bottazzo et al. [3] reported the presence of antibodies to the islet cells in blood samples from people with insulin-dependent diabetes.

Together, these observations prompted a radical revision in the understanding of diabetes. The prevailing model of diabetes as a single disorder that could present either in childhood (juvenile onset) or later in life (adult onset) was replaced by a classification that clearly distinguished type-2 diabetes (then almost exclusively a disorder of later adulthood) from type-1 diabetes. Type 1 became known as autoimmune diabetes, caused by a dysregulated immune system that attacks, and ultimately destroys, the p cells.

The past three decades have seen an exponential rise in the incidence of diabetes - most noticeably of type 2, owing to the greater numbers involved, but also of type-1 diabetes. While type-2 diabetes is widely understood to be linked to obesity and the insulin resistance it causes, the rise in type 1 has not been satisfactorily explained.

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