Type 1 diabetes occurs as the result of autoimmune destruction of beta cells in the pancreas. This attack arises in part through autoreactive B lymphocyte presentation of islet antigens to cognate T lymphocytes. Dr. Rachel Bonami’s research is focused on understanding how these cognate T-B interactions can be disrupted to prevent type 1 diabetes. Islet autoantibodies, the product of these interactions, serve as biomarkers for disease risk. The presence of insulin autoantibody is particularly predictive of disease onset in young patients, highlighting insulin as a critical autoantigen in this disease process. Dr. Bonami has shown that anti-insulin B lymphocytes can be selectively eliminated using a monoclonal antibody to prevent type 1 diabetes in a preclinical model. This work received a Faculty of 1000 recommendation and suggests that such an approach holds promise for the prevention of type 1 diabetes without exposing patients to broad immunosuppression. Dr. Bonami’s work has also focused on identifying and correcting defects in immune tolerance mechanisms in the setting of autoimmune disease. She was previously awarded a postdoctoral fellowship by the Juvenile Diabetes Research Foundation and was invited to present her work at Keystone Symposia and at the American Association of Immunologists annual meeting. In 2015 the Vanderbilt Diabetes Research and Training Center presented her with the Daryl K. Granner Scholar in Diabetes Postdoctoral Fellow Award, Ph.D..