Assistant Professor of Pathology, Microbiology, and Immunology

Assistant Professor of Medicine

Research Description
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.
 

Assistant Professor of Medicine

Research Description

Dr. Dean's longtime interests have been to understand how nutritional status and other environmental factors stimulate cell proliferation and affect the susceptibility of vulnerable cells to degeneration. Her current interests are the determinants of endocrine mass, specifically pancreatic islet alpha cell mass. While much effort has been focused on understanding beta cell biology because of insulin's well known role in diabetes, very little is known about signals regulating other islet cells. Alpha cells secrete glucagon in response to hypoglycemia, but persons with diabetes have hyperglucagonemia contributing to hyperglycemia. Struck by the impressive alpha cell hyperplasia and hyperglucagonemia in mice with interrupted glucagon signaling, Dr. Dean sought to identify the mechanism underlying this during her postdoctoral training. She identified that unknown circulating factors stimulate alpha cell hyperplasia in mice with interrupted glucagon signaling. She then collaborated with multiple investigators at Vanderbilt and other institutions to identify that these circulating factors are amino acids defining a novel hepatic-pancreatic islet alpha cell axis. She demonstrated that this effect is conserved in human alpha cells suggesting that this axis is relevant to human biology and disease. Her current interests are 1) to define the mechanism of how amino acids are sensed by alpha cells to stimulate proliferation and glucagon secretion and 2) to investigate the role of amino acids on alpha cell dysfunction in diabetes.

Assistant Professor of Medicine

Research Description

Dr. Robinson-Cohen’s empirical work has been in the areas of cardiovascular, clinical, and genetic epidemiology. She mainly focuses on understanding risk factors for and consequences of mineral metabolism disturbances in the general population and in chronic kidney disease. She is also interested in identifying risk factors and potential treatment options to address the disproportionate burden of cardiovascular disease in the setting of chronic kidney disease.

Associate Professor of Medicine, Department of Medicine, Division of Infectious Diseases

Research Description

The Serezani laboratory aims to develop therapeutic strategies to control systemic (sepsis) and localized infections (skin and lung) in healthy individuals, individuals with immune deficiencies, and those suffering from chronic inflammatory diseases, such as diabetes. We have concentrated much of our efforts in understanding the role of the lipid mediators leukotriene B4 and prostaglandin E2 and their actions on microRNAs, epigenetic changes and phosphatases to modulate immune cells involved in the control of microbial infection in these different contexts. Our lab employs state of the art techniques to understand in vitro and in vivo cellular and microbial dynamics, such as intravital microscopy and IVIS imaging, along with different fluorescent and cell-specific deficient mice to track cell and organ-specific events.