Endocrine Abstracts

Type 1 diabetes (T1D) is a T-cell mediated autoimmune disease in which the insulin-producing pancreatic beta-cells in the islets of Langerhans are destroyed. While the symptoms of the disease have become treatable to a certain extent, even intensive state-of-the-art insulin therapy cannot prevent the development of severe complications in the majority of patients. There is, therefore, a huge and unmet clinical demand for disease intervention, but a cure for T1D does not yet exist. Current therapy combats disease symptoms, not its cause. Disease intervention therapies directed against T-cells have been shown to halt the disease process and delay recurrent beta-cell destruction after islet transplantation. However, the success rate depends on the beta-cell mass and immune status at time of intervention therapy. Induction or restoration of immunological self-tolerance should be achieved to revert the autoimmune processes leading to beta-cell destruction permanently, preferably before clinical manifestation of the disease, at the time that the beta-cell mass still suffices to maintain normoglycemia. The challenge is to determine which immune factors associate with beta-cell destruction or tolerance, and to define what measures can suppress autoreactivity.