Dr. Lee obtained his medical and graduate degrees from Duke University School of Medicine under the mentorship of Dr. Barton F. Haynes. Dr. Lee pursued post-graduate medical training (internship, medical residency and Rheumatology fellowship) at Brigham and Women’s Hospital, Harvard Medical School. His fellowship research, which focused on molecular mechanisms of autoimmune arthritis pathogenesis, was primarily mentored by Dr. Michael B. Brenner. After completing his fellowship in Rheumatology, Dr. Lee joined the faculty at Brigham and Women’s Hospital. The Lee laboratory is focused on understanding autoimmune and inflammatory mechanisms that contribute to arthritis. The laboratory studies mechanisms of joint inflammation in both mouse models of disease and in human specimens obtained from patients with rheumatoid arthritis. Two thematic foci in his laboratory include: a) the role of autoantibodies interacting with components of the innate immune system in arthritis pathogenesis and b) molecular mechanisms governing the behavior of synovial tissue (fibroblast-like synoviocytes) in arthritis. These studies have identified participation of multiple innate immune lineages as well as their pro-inflammatory products in arthritis pathogenesis. More specifically, his work has shown that mast cells stimulated by autoantibodies contribute to arthritis severity by generation of cytokines and by releasing their granule contents and that neutrophils can promote synovial inflammation by release of eicosanoids. Furthermore, Dr. Lee’s research has provided insight into the involvement of synovial fibroblasts (and thus synovial tissue) in arthritis pathophysiology through studies of the adhesion molecule cadherin-11. This line of investigation highlights the importance of the synovial tissue response to autoimmune inflammation in the disease activity of inflammatory arthritis.