Antigen-specific therapy against type 1 diabetes: mechanisms and perspectives

Type 1 diabetes (T1D) is an immune-mediated disease that occurs when the insulin-producing β‑cells of the pancreatic islets are destroyed by an inflammatory process perpetuated by cells of the immune system. The logical approach to suppress T1D is to inactivate or eliminate the lymphocytes responsible for inducing inflammation and targeting the β‑cells. Antigen-specific approaches have been devised and were able to target inflammatory lymphocytes and induce apoptosis or block trafficking to pancreatic islets. Lack of costimulation, expansion of Tregs and bystander suppression are likely mechanisms by which antigen-specific treatments modulate pathogenic T cells. This strategy, however, while prevents the onset of T1D, could not overcome overt T1D, perhaps because of collateral damage to the islet vascular network. Recent developments indicate that donor endothelial stem cell precursors can repair the islets' vascular niche and assist antigen-specific therapy against overt T1D.