| Project/Area Number |
62570547
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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 |
Hematology
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| Research Institution | Osaka University |
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Principal Investigator |
TAGAWA Shinichi Research Assistant Division of Internal Medicine, Department of Clinical Research, The Research Institute for Microbial Diseases, Osaka University., 微生物病研究所臨床部門, 助手 (70171569)
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| Co-Investigator(Kenkyū-buntansha) |
KITANI Teruo Professor Division of Internal Medicine, Department of Clinical Research The Res, 微生物病研究所臨床部門, 教授 (80028406)
中村 善尚 大阪刑務所, 法務技官
TOKUMINE Yokihiro Research Assistant Division of Internal Medicine, Department of Clinical Researc, 微生物病研究所臨床部門, 助手 (90207564)
NAKAMURA Yoshihisa Technical Staff Mivistry of Justice Osaka Prison
脇 耕二 大阪大学, 微生物病研究所, 医員
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | LAK / LAK-CF / LGL / NK-CF / IL-2 / IL-2レセプター / LAK特異抗体 / LAK由来細胞障害因子 / LGL白血病 / p55 / p75 / Tac抗原 |
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| Research Abstract |
We detected by making monoclonal antibody specific for the leukemic LGL cells with LAK activity that there was antigen, we designated as LH49, on the surface of the leukemic cells from the patient with LGL leukemia mediating LAK activity. The LH49 antigen was not detected on the surface of leukemic cells from a patient with LGL leukemia without LAK activity. We also found that 30 % of peripheral mononuclear cells were reactive with this monoclonal antibody, LH49. We found that the culture supernatant of the clone did suppress neither the NK function mediated by peripheral mononuclear cells obtained from normal donors nor the LAK activity mediated by the leukemic LGL cells. Thus, the role of the LH49 antigen for the NK and LAK function must be clarified in the future using purified monoclonal antibody, LH49, from ascitic fluid.
We found that the leukemic LGL cells of the patient released LAK-CF when they were co-cultivated with stimulator cells. The LAK-CF activity was parallel with the LAK activity detected as a cell mediated killing function. Furthermore, we found that the target cell killing spectrum of the LAK-CF and NK-CF were different. Chemical analysis of the LAK-CF revealed that a substance of molecular weight of 20 kd was responsible for the function. However, judging the data obtained from ionexchange chromatography, it became clear that the soluble factor was not composed from single substance.
It is generally accepted that p55 Tac antigen appears on the surface of T cells and NK cells when they have been stimulated by IL-2 or antigens. The reason was not clear, however, why peripheral T cells obtained from normal donors and leukemic LGL cells in which Tac IL-2 receptors have not been detected are activated by IL-2 to become LAK. Using chemical crosslinking methods and iodinated IL-2, we newly found that there is a second IL-2 receptor, p75, on the surface of LGL leukemia cells.
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