Kei Yasuda, PhD
|Institution||Boston University School of Medicine|
|Address||650 Albany St Evans Biomed Research Ctr|
Boston MA 02118
|Institution||Boston Medical Center|
“To the clinician, systemic lupus erythematosus is important because it is a potentially fatal disease that is easily confused with many other disorders. To the immunologist, lupus is intriguing because all the key components of the immune system are involved in the underlying mechanisms of the disease.”(Anisur Rahman, Ph.D., and David A. Isenberg, M.D. N Engl J Med. 2008 Feb 28;358(9):929-39.)
I have studied this devastating but intellectually challenging disease more than 10 years. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of great diversity of autoantibodies against nucleic acids (DNA and RNA) and other autoantigens. The autoantibodies form immune complexes that deposit in various tissues including the kidney, causing inflammation and end-organ damage. Current medications are only partially effective and have severe side effects.
We are interested in the role of interferon regulatory factor-5 (IRF5) in the pathogenesis of SLE in mice and humans. We have shown 1) IRF5 in plasmacytoid dendritic cells is involved in the production of type I interferons (IFNs), which are pathogenic cytokines in SLE, and 2) IRF5 contributes to the formation of antibody-producing plasma cells in lupus-prone mice. Currently we investigate how IRF5 is involved in the plasma cell development and T cell differentiation. Although there is no doubt that IRF5 is a potential target, “IRF5 inhibitors” for the treatment of SLE are not available at the moment. I seek collaborations to accelerate the development of potential drugs to cure SLE.
My recent interest is neutrophil activation induced by immune complexes. Studies have shown that neutrophils release reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) upon stimulation with RNA-containing immune complexes. My new goal is to investigate whether other immune complexes can activate neutrophils, and what kind of signaling pathways are involved in the activation.
- Systemic lupus erythematosus
- Interferon regulatory factor-5
- plasmacytoid dendritic cells
- plasma cells
- Toll-like receptor-7
- Toll-like receptor-9
- autoimmune disease
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