Our research focuses on the cellular and molecular context of aberrant DNA and RNA recognition in autoimmune diseases such as systemic lupus erythematosus (SLE). In particular, we are currently interested in key questions such as: How does the structure of secondary lymphoid organs influence the induction of tolerance to apoptotic cells versus the initiation of autoimmune reactions? What changes do DNA or RNA from apoptotic cells undergo during disease, and how do these modifications change DNA or RNA recognition by nucleic acid sensors and downstream signaling? To address these questions, we use a combination of cellular and molecular analyses, mouse models, and studies of patient samples. Answers to these questions will help to dissect complex autoimmune diseases into pathophysiological subtypes, with the ultimate goal to identify patient-specific pharmacological interventions.