Does immune-tolerance treatment with Alum-formulated GAD65 protect insulin-production in the pancreatic islet β cells?

Abstract

Type 1 diabetes is a serious chronic disease in which the pancreatic islet beta cells are destroyed by autoimmunity specifically directed to intracellular autoantigens. Still undefined environmental factors are likely to initiate the disease process. One of the autoantigens is glutamic acid decarboxylase (GAD65) and attempts are made to induce immunological tolerance against this autoantigen. Alum-formulated GAD65 (Diamyd^®) has been given subcutaneously in two injections with one month apart to recent onset type 1 diabetes patients with positive GAD65 autoantibodies. The injections were found to preserve residual β-cell function without treatment related serious adverse events. Phase III studies in children with recent onset type 1 diabetes are ongoing along with a study (DIAPREV-IT) aimed at testing whether Diamyd^® may prevent the clinical onset of diabetes in non-diabetic children with GAD65 autoantibodies and at least one more islet autoantibody. Future studies may include investigation of Diamyd^® in combination with other immunomodulating autoantigens.