Rachel H. Bonami, PhD
Assistant Professor of Medicine, Division of Rheumatology and Immunology
Autoimmune diseases are frequently marked by autoantibodies, which signal immune tolerance checkpoint breach by autoreactive B cells. We do not fully understand the immune system “glitches” that push B lymphocytes to inappropriately respond to autoantigens, engage autoreactive T cells, and/or morph into autoantibody-secreting cells. Dr. Bonami’s translational research program takes advantage of access to several unique clinical cohorts (e.g. Type 1 Diabetes TrialNet and Myositis, Scleroderma Treatment Initiative Center (MYSTIC)) and cutting-edge hybridoma and single-cell RNAseq/CITEseq/BCRseq technology to address these critical questions. Her laboratory is also applying these techniques to investigate a new autoimmune syndrome resembling Sjogren’s syndrome that can occur in cancer patients treated with checkpoint inhibitors. Her lab interweaves wet-lab experimental approaches with computational analyses to define B cell phenotypic and immune repertoire changes associated with these autoimmune processes.
Autoantibodies are used clinically to predict or diagnose many autoimmune diseases. Autoantibodies can be directly pathologic and/or signal interactions between autoantigen-specific B and T cells that underly tissue damage. Dr. Bonami’s research program focuses on identifying autoantigen-specific B cells to define their phenotypic and functional attributes in people at risk for type 1 diabetes, patients with spontaneous autoimmune diseases such as myositis and Sjogren’s syndrome, and patients who develop autoimmunity following immune checkpoint inhibitor therapy. Our goals are to: Develop approaches to harness autoreactive B cells as more selective biomarkers; and identify pathways to target to limit autoreactive B cell survival and function.