The department of Clinical Immunology and Rheumatology was established at Hiroshima University Hospital in 2009. Rheumatologists in this department are experts in the diagnosis and management of all types of arthritis including rheumatoid arthritis, crystalline arthritis, as well as such complex connective tissue disorders as systemic lupus erythematosus, systemic vasculitis, myositis and scleroderma. In addition, we are involved in clinical trials and research that seek to advance treatment for these diseases.

Work in our laboratory is focused on the synovial cell. Synovial cells play important roles in the disease progression of rheumatoid arthritis (RA). The cells proliferate to be a major component of pannus, a granulomatous tissue observed in RA. Synovial cells produce cytokines and chemokines that contribute to chronic inflammation of affected joints of RA, and also secrete proteinases that cause degradation of joint tissues, including bone and cartilages, which lead to severe structural destruction of inflamed joints.

By using synovial cell isolated from RA patients, we examine the functions of the cell. One of our current focuses is the proliferation of synovial cells. Synovial cells in RA often express proto-oncogenes (e.g. Myc, Ras, mutant p53). These genes have a potential to regulate the proliferation of synovial cells. Especially, we focused on Survivin and its splicing variants. We reported that Survivin-2B (variant protein) is abundantly expressed and has a significant role for cell proliferation in synovium from RA patients.

We also analyze the effect of synovial cell in regulating osteoclastogenesis. There seems soluble inhibitory factor for osteoclastogenesis in the supernatant of cultured synovial cell. We attempt to identify the molecule that blocks osteoclast formation in inflamed joint. These researches might help us to inhibit bone erosion or restore destructed bone in RA.

And more, we are trying to develop a method that prevents articular cartilage destruction in RA. When cartilage becomes damaged, it can't heal itself like other components in the body. Then, the goal is to find some new ways to prevent cartilage defect from inflamed synovium. We focused on WWP2, a cartilage specific E3 ubiquitin ligase, which have a cartilage protective function. Replacement of WWP2 might be a novel treatment method to block cartilage damage in RA joint.