Rachel Henry Bonami, Ph.D.
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B cell, T cell, autoimmunity, type 1 diabetes, arthritis, microbiome
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..
Research Information
Dr. Bonami has received a grant from the Juvenile Diabetes Research Foundation (JDRF). This is a 3-year Strategic Research Agreement. Here is a summary of her research project: Abnormalities in the immune system are present long before Type 1 diabetes is diagnosed in the clinic, as indicated by the early presence of islet autoantibodies in the pre-symptomatic stages of the disease. We do not yet understand the immune system glitches that push B lymphocytes to inappropriately respond to islet autoantigens, engage autoreactive T cells, and morph into autoantibody-secreting cells. Our objectives are: 1) To immunologically define how B lymphocyte recognition of beta cells evolves during the early stages of disease, and 2) To discover which B lymphocyte subsets harbor insulin autoimmunity during the pre-symptomatic period. We expect this information about the early disease process to highlight novel characteristics of B lymphocytes to target for T1D prevention.
