Mechanisms of the anergy of T cells induced by varient types of soluble VCAM-1
Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants|
|Research Institution||Kagoshima University|
MATSUYAMA Takami Faculty of Medicine Kagoshima University, Professor, 医学部, 教授 (30145479)
|Project Period (FY)
1997 – 1998
Completed(Fiscal Year 1998)
|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)
|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|
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.
Research Products (5results)