Ian R. Rifkin, M.D., Ph.D.

Associate Professor of Medicine and Virology, Immunology & Microbiology
650 Albany Street
Office: X514; 617-638-7325
Lab: E-5; 617-414-3338

M.D.  University of the Witwatersrand, South Africa
Ph.D. University of Cambridge, England

See BU Profile for additional information and publications.

There are two main research aims in my 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.  We mainly use mouse models and in-vitro systems for these studies, although we 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 our original observation that dendritic cell activation by nucleic acid autoantigen-containing immune complexes occurs through the dual engagement of an Fc receptor and a Toll-like receptor (TLR9 for DNA autoantigens and TLR7 for RNA autoantigens).  Ongoing studies aim to characterize the precise nature of the stimulatory autoantigens in more detail, 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 recently been identified as a major susceptibility gene for SLE in humans and plays an important role in TLR signaling.  We are using a combination of in vivo and in vitro approaches to evaluate the biological role of IRF5 in SLE.

The second main aim of our research is to determine the mechanisms responsible for the premature atherosclerosis seen in SLE.  Premature atherosclerosis is a major cause of morbidity and mortality in patients with SLE, although the lupus-specific risk factors responsible for this are poorly understood.  In collaboration with Dr. Walsh in Molecular Cardiology, we 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.