Shinichi Sato, M.D., Ph.D.

Japan
Professor and Chairman, Department of Dermatology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan
I graduated from the University of Tokyo in 1989 and obtained MD and PhD degrees from the University of Tokyo. I have been working mainly on basic and clinical aspects of systemic sclerosis, a systemic autoimmune disorder. To clarify the pathogenesis of systemic sclerosis from the viewpoint of B lymphocytes, I studied molecular and cellular biology of B cells at Department of Immunology, Duke University Medical Center under the supervision of Professor Thomas F. Tedder from 1994 to 1997. My study was the first to reveal that CD19, a critical signal transduction of B cells, regulates autoimmunity. After returning to Japan as Assistant Professor at Department of Dermatology, Kanazawa University in 1997, I found intrinsic B cell abnormalities due to CD19 overexpression in systemic sclerosis. In 2004, I was promoted to Professor and Chairman, Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences. I expanded my work on systemic sclerosis and moved to Professor and Chairman, Department of Dermatology, the University of Tokyo in 2009. Based on the results of the studies using human systemic sclerosis patients, we conducted “investigator-initiated” double-blind, parallel-group comparison, clinical trial of rituximab in patients with SSc (the DESIRES study). This randomized, double-blind, placebo-controlled study demonstrated that rituximab treatment is effective for skin and lung fibrosis in SSc. This is the “first” study to reveal significant difference relative to placebo with skin score as the primary end point in SSc. Rituximab was approved for SSc in Japan on Sep, 2021 ahead of other countries. and show that B cell depletion therapy by anti-CD20 antibody is effective for systemic sclerosis. Furthermore, we are currently performing various clinical trials for SSc using anti-IL-17RA antibody, anti-CD19 antibody, anti-IL-23p19 antibody, and anti-IL-31RA antibody.