Ian Rifkin, M.D.
There are two main research aims in Dr. Rifkin’s laboratory. The first aim is to understand the pathogenesis of the systemic autoimmune disease systemic lupus erythematosus (SLE), with the ultimate goal of identifying new therapeutic targets. His laboratory mainly We mainly uses mouse models and in vitro systems for these studies, although they also work with human cells and patient material. Specific projects include: 1) Studying mechanisms and signaling pathways responsible for the activation of dendritic cells in SLE. This project is based on the original observation that dendritic cell activation by nucleic acid auto antigen-containing immune complexes occurs through the dual engagement of an Fc receptor and TLRs (TLR9 for DNA auto antigens and TLR7 for RNA auto antigens). This work is in collaboration with Dr. Greg Viglianti. Ongoing studies aim to characterize the precise nature of the stimulatory auto antigens and to determine the overall contribution of TLR-mediated dendritic cell activation to SLE pathogenesis. 2) Determining the role of interferon regulatory factor 5 (IRF5) in lupus pathogenesis. IRF5 has been identified as a major susceptibility gene for SLE in humans and plays an important role in TLR signaling. His laboratory is using a combination of in vivo and in vitro approaches to evaluate the biological role of IRF5 in SLE. The second main aim of his research is to determine the mechanisms responsible for the premature atherosclerosis seen in SLE. In collaboration with Dr. Walsh they have developed a novel mouse model of premature atherosclerosis and SLE, and are using this model to explore underlying pathogenic mechanisms and test new therapeutic approaches.