| Project/Area Number |
09670483
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | Kagoshima University |
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Principal Investigator |
MATSUYAMA Takami Faculty of Medicine Kagoshima University, Professor, 医学部, 教授 (30145479)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Soluble VCAM-1 / Intracellular Signals / IL-2 Nuclear Factors / Calmodulin dependent kinase II / Chemotaxis / シグナル伝達 / 自己免疫 / アネルギー / カルモデュリンキナーゼ / 関節液 / IL-2 |
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| Research Abstract |
1. We examined how soluble VCAM-1 affects the pathway of signal transduction in Jurkat cells induced by the stimulation of TCR/CD3 molecules.
1) Addition of soluble VCAM-1 to stimulated Jurkat cells inhibited the binding of Ap-1, NF-AT and Oct-I to the IL-2 promotor region but not that of NF-kB.
2) Soluble VCAM-1 induced the activity of calmodulin dependent kinase II but not the phosphorylation of focal adhesion molecule in stimulated Jurkat cells.
3) The chemotaxis of T cells by soluble VCAM-1 was dependent on the activity of rho, protein kinase C, and calmodulin dependent kinase II.
2. Previously, we reported that soluble VCAM-1 acts inhibitory on the functions of T cells. In the present experiments, it was fount that soluble VCAM-1 play the following roles in the functions of T cells.
1) Soluble VCAM-1 inhibited the function of CD45RO^+ T cells as compared that of CD45RO^- T cells.
2) Soluble VCAM-1 induced the chemotaxis of IL-2 dependent T cell lines, synovial fluid T cells from rheumatoid arthritis patients and Jurkat cells.
3. We developed a dimer form of soluble VCAM-1 by connecting cDNA of soluble VCAM-1 with cDNA of IgGFc portion.
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