University of Virginia Health System

The main focus of my research is to understand how autoantibody responses against lupus-associated autoantigens are initiated and sustained. Using mice transgenic for human class II proteins, we are exploring the hypothesis that T cell repertoire against lupus-associated antigens is shaped through multiple encounters with pathogenic microorganisms harboring molecular mimics of these autoantigens. Thus, molecular mimicry at T cell epitope level plays an important role in initiating autoantibody responses in SLE. Once initiated, in a genetically susceptible individual the autoimmune responses are sustained through the process of epitope spreading. We are currently involved in identifying the mechanisms and the contributions of non-MHC genetic loci in epitope spreading. We are also exploring the use of novel immunotherapeutic agents to regulate the epitope spreading process.