Type 1 Diabetes (T1D) is an autoimmune disease characterized by the body’s immune cells, including T cells and potentially natural killer (NK) cells, attacking the insulin-producing pancreatic β-cells. This investigation seeks to examine how two costimulatory proteins, CD226 and TIGIT, responsible for the immunoregulation of immune cells, can be modulated to develop new therapeutic approaches to treat T1D. To evaluate this costimulatory pathway in the context of translational medicine applications, I will be examining the therapeutic potential of isolating CD226 deficient Human Regulatory T cells (Tregs) for use in adoptive cell therapies, as well as the potential of CD226 monoclonal antibody therapies using the NOD mouse model.