| Project/Area Number |
04557020
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| Research Category |
Grant-in-Aid for Developmental Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Hokkaido University |
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Principal Investigator |
UEDE Toshimitsu Hokkaido University, Institute of Immunological Science, Professor, 免疫科学研究所, 教授 (00160185)
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| Co-Investigator(Kenkyū-buntansha) |
SUDO Tetsuo Toray Industries, Inc., Basic Research Laboratories, Principal Researcher, 基礎研究所, 主任研究員
YASUDA Keisyu Hokkaido University, Department of Medicine University Hospital, Professor, 医学部・付属病院, 教授 (60125359)
須藤 哲夫 東レ株式会社, 基磯研究所, 主任研究員
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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 |
¥17,100,000 (Direct Cost: ¥17,100,000)
Fiscal Year 1994: ¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 1993: ¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 1992: ¥7,600,000 (Direct Cost: ¥7,600,000)
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| Keywords | Transplantation / Rejection / Cell Adhesion Molecule / Immunological Torerance / CTLA4 / 可溶性接着分子 / 補助シグナル / アナヅィー / アナジィー |
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| Research Abstract |
The purpose of this study was to generate soluble forms of cell adhesion molecules which can efficiently inhibit the costimulatory signals for T cell activation and proliferation. We generated a fusion protein consisting of a Fc portion of human IgG_1 or human IgM and an extracellular portion of mouse CTLA4 (CTLA4-IgG and CTLA4-IgM,respectively).
CTLA4-IgM efficiently inhibited the T cell proliferation induced by mixed lymphocyte reaction (MLR) as compared to CTLA4-IgG.Furthermore, the combination of low does FK506 and CTLA4-IgM (2.3mug/ml) resulted in significant prolongation of cardiac allograft surviral (C57BL/6 into CBA/J), where as cardiac alloglaft surviral in recipients treated with FK506 plus CTLA4-IgG (2.3mug/ml) resulted in moderate prolongation of grafts.
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