The immune system consists of a highly specialized group of cells involved in the elimination of invasive pathogens and in preventing attack against self-tissue, thus preserving the integrity of the organism. Among these cells, regulatory T cells (Tregs), play a crucial role in preventing autoimmunity, by limiting the immune response against self-tissues. In Type I diabetes, immune cells mistake the body's own insulin-producing cells for foreign cells and destroy them. Tregs in this autoimmune disease seem not to work appropriately in controlling the immune response. In Dr. Vignali's lab we are especially interested in understanding why Tregs fail to control autoimmunity, focusing on proteins involved in stabilizing Tregs. Conducting in vitro and in vivo studies in non-obese diabetic mice, I am studying the role of the protein Neurophilin-1 in Treg stability and function in this disease. Specifically, we hope to reveal the signaling pathways and ligands important to the function of that protein. This work could lead to the development of drugs to modulate immune system function as a therapeutic approach to activate Tregs to treating Type I diabetes.