Type 1 diabetes (T1D) involves a complex genetic predisposition, including over 40 genes that have been identified to confer susceptibility to disease. In addition, the disease process appears susceptible to environmental factors (diet, bacteria, viruses). Increasing evidence suggests that T1D patients exhibit defective control of immune responses. Despite the large number of genes identified, the cellular and molecular contributors to the disease process remain poorly characterized. Our laboratory seeks to understand how genes and environmental inflammatory stimuli (infections) cause a breakdown in the processes that normally control immune tolerance to islet beta cells. In order to conduct these studies, we collect and analyze blood samples form patients with T1D. We also study cells and tissues from a collaborative network referred to as the nPOD program.