| Project/Area Number |
04670378
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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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 | University of Tokyo |
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Principal Investigator |
INOUE Tetsufumi University of Tokyo, Department of Medicine, Associate Professor, 医学部(病), 講師 (30092141)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Kenji University of Tokyo, Department of Medicine, Assistant Professor, 医学部(病), 助手
TOMA Shigeto University of Tokyo, Department of Medicine, Assistant Professor, 医学部(病), 助手 (50207528)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | LFA-1 / ICAM-1 / CD44 / IL-10 / IL-2 / IL-2 receptor / 慢性関節リウマチ / ヒアルロン酸 / IL-6 |
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| Research Abstract |
Expresssion of LFA-1, ICAM-1, and CD44 molecules on peripheral blood T lymphocytes were studied. No differences were found between RA patients and healthy individuals. Effects of several therapeutic drugs for RA on the expression of thode molecules were also analized. In the series of experiments, dexamethasone clearly decreased the expression of ICAM-1, suggesting the possibility that anti-rheumatic drugs showed their clinical effects through the modification on such molecules.
Anti CD44 antibodies enhanced the release of IL-2 and IL-6 from activated T lymphocytes. Aggregation of cells by anti-CD44 antibodies was also observed in the culture, indicating that CD44 molecules showed the role of signal transmission through bringing T lymphocytes in contact with each other.
IL-10 enhanced the proliferation and differentiation of activated B lymphocytes in the presence of IL-2, by means of the accelerated expression of IL-2 receptor molecules.
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