| Project/Area Number |
03454220
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Saitama Medical Center, Saitama Medical School |
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Principal Investigator |
ABE Tohru Saitama Medical Center, Saitama Medical School 2nd Department of Medicine. Professor, 医学部, 教授 (60051207)
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| Co-Investigator(Kenkyū-buntansha) |
AMANO Koichi Saitama Medical Center 2nd Department of Medicine, 医学部, 助手 (00175928)
KOIDE Jun Saitama Medical Center 2nd Department of Medicine Assistant Professor, 医学部, 講師 (70178193)
TAKEUCHI Tsutomu Saitama Medical Center 2nd Department of Medicine Associate Professor, 医学部, 助教授 (50179610)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1992: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | rheumatoid arthritis / T cell phosphorylation / PDGF / zata chain / CD44 antigen / CD44抗原 / 線維芽様細胞 / 血小板由来増殖因子 / CD3分子 / T細胞 / 燐酸化 |
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| Research Abstract |
For the past years, we have studied to clarify the pathogenesis of rheumatoid arthritis. We focused our attention to T cells and synovial cells. Firstly we examined phosphory-lation of CD3-Ti complex in order to identify possible causative agents. If there is specific agent(s) to initiate RA, such specific antigenic stimuli must phosphorylate zata chain of CD3-Ti complex. To our surprise, there was no phosphorylation of zata chain in T cells from synovial membrane, indicating that no specific antigen is considered to cause RA. Secondary, we examined synovial type A cells. The cells could become multi-nucleated cells in the presence of anti-DR antibody in culture medium. The multi-nucleated cells had osteoclastic activity which indicated that such cells play crutial role for bone destruction in patients with RA. Lastly, we examined synovial type B cells. We established cloned type B cells. The cells expressed CD44 molecule on the cell surface. The cells proliferated in the presence of PDGF in culture medium. These evidences clearly indicate that various cells in synovial membrane participate for the formation of rheumatoid inflammation.
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