​ Dr. Gary Firestein’s work focuses on the pathogenesis and treatment of rheumatoid arthritis. His lab mapped the synovial cytokine profile of RA and demonstrate the dominance of macrophage and fibroblast products. These studies played a pivotal role in the development of the highly effective anti-TNF and other anti-cytokine approaches to RA. He has also dissected the kinome in RA synoviocytes and used this technology to identify and validate novel therapeutic targets. Recently, Dr. Firestein has mapped the epigenetic profile of the RA synovium and identified a unique DNA methylation signature in rheumatoid synoviocytes.

Dr. Firestein received his AB from Harvard College and MD from Johns Hopkins. After training in internal medicine at UCLA, he completed his fellowship in rheumatology at UCSD. He has served on the faculty at UCSD since 1996 and was chief of the Division of Rheumatology, Allergy and Immunology from 1998-2010. He currently serves as the Dean and Associate Vice Chancellor for Clinical and Translational Research at UCSD.

Dr. Firestein has  studied the role of aggressive synoviocyte behavior in RA as a mechanism of joint destruction and implicated tumor suppressor genes mutations in the pathogenesis of disease. Over the last decade, his laboratory has worked extensively on signal transduction pathways as potential therapeutic targets. These studies identified key signaling molecules regulating synovial inflammation and paved the way to several effective oral small molecule inhibitors that are currently in late phase clinical development for RA. More recently, Dr. Firestein has focused on epigenetics and discovered a DNA methylation signature specific to RA. In addition, he directed a number of innovative clinical studies for the treatment of rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, scleroderma, and autoinflammatory syndromes with a focus on developing novel biomarker endpoints. His group developed novel biomarker studies using serial synovial biopsy studies in RA to understand the mechanism of action for anti-rheumatic agents.

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