| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Research Abstract |
I investigated about the role of neuroendocrine-immune system in autoimmune disease. I found that synovial cells and T cells in patients with rheumatoid arthritis (RA) produced prolactin, IL-6 and TNFα. Prolactin induced TNFα, IL-6 and IL-8 production from RA synovium and enhanced proliferation of fibroblast-like synovial cells. Prolactin induced MMP-3 production and inhibited TIMP-1 production in RA synovial cells. Prolactin receptors were expressed in the surface of macrophage-like synovial cells, fibroblast-like synovial cells, and synovium-infiltraring T cells. Bromocriptine, which inhibites the secretion of prolactin from endocrine cells and immune cells, inhibited prolactin production in RA synovium, and then IL-6,IL-8 production in RA synovium. Bromocriptine also inhibited RA synovial cell proliferation. These results suggested that prolactin involved bone-carilage distruction in RA pathgenesis. I found that NGF involved the pathogenesis in RA synovium.
Furthermore, I studied the expression of hormome and neuropeptides in RA synovium and their production in serum in patients with RA, systemic lupus erythematosusu (SLE), and vasculitis. I found the presence of Growth hormone, TRH, and TSH producing cells in RA synovium. Growth hormone, prolactin and IGFBP-3 production increased in serum in some patients with RA, SLE and vasculitis.
These results suggested that neuroendocrine-immune system involved the pathogenesis in autoimmune disease. Further examination is necessary about them.
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