Maria Bettini Lab


t cellsThe focus of research in my laboratory are the mechanisms of tolerance and their failure in autoimmunity. In order to understand pathways leading to immune dysregulation we are using a combination of innovative mouse models of T cell biology and autoimmunity, including mouse and human single T cell receptor “retrogenic” mice. Past and current projects investigate the how T cell receptor antigen specificity and affinity effect the function of pathogenic and regulatory T cells in autoimmune type 1 diabetes. The ultimate goal is to identify basic mechanisms of autoimmunity and apply this knowledge toward discovery of therapeutic targets for treatment or prevention of autoimmune disorders. In our past NIH funded studies we have shown that T cell receptor self-reactivity plays an important role in tissue specific response by modulating the type and amplitude of regulatory T cell suppressive mechanisms necessary for protection against autoimmune diabetes (JCI Insight 2018; Cutting Edge J Immunol2018). More recently, we have shown that self-antigen expression promotes tolerance through parallel mechanisms of Foxp3+ Treg development, deletion of high affinity T cells, and reduction in pathogenicity of self-reactive T cells that escape thymic selection (Bettini et al., Diabetes 2020). These processes critical for self-tolerance are disrupted in responses to alternatively processed proteins or neo-antigenic targets of autoimmunity (Liu et al., 2020, Diabetes).

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Maria Bettini
Maria Bettini, PhD
Associate Professor
Microbiology & Immunology


Department of Pathology
Division of Microbiology and Immunology
University of Utah
Emma Eccles Jones Medical Research Building
15 N. Medical Drive East, Rm 1420A
Salt Lake City, UT  84112
phone 801-585-6421