| Project/Area Number |
06454594
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
NAGASAWA Shigeharu Hokkaido Univ., Fac.of Pharm.Sci., Prof., 薬学部, 教授 (70029958)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Yusuke Hokkaido Univ., Fac.of Pharm.Sci., Assist., 薬学部, 教務職員 (10250466)
NISHIMURA Hitoshi Hokkaido Univ., Fac.of Pharm.Sci., Assist., 薬学部, 助手 (80241347)
TAKAHASHI Kazuhiko Hokkaido Univ., Fac.of Pharm.Sci., As Prof., 薬学部, 助教授 (10113581)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1995: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1994: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | COMPLEMENT / PHAGOCYTES / APOPTOSIS / IMMUNE RESPONSE / POSONIZATION / RECEPTORS / 抗体レセプター / 活性酸素 |
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| Research Abstract |
We investigated the biological functions of the complement system, which acts as a host defense for invading cells.
The important results obtained bu this project are as follow ;
1.Activation of the autologous alternative complement pathway by apoptotic cells. Complement activation does not occur on homologous live cells. We observed the activation of alternative human complement pathway by human umbilical vein cells, when these cells died of apoptotic process. This autologous complement activation by apoptotic cells was also observed with apoptoticJurkat cells, a human T cell line. these findings suggest that novel proteins should be expressed at the surface of apoptotic cell to induce autologouscomplement activation. Complement activation results in the opsonization oftarget cells with C3b derivative, iC3b. Phagocytes sugh as macrophages express C3 receptor and can phagocytose iC3b-coated cells. So, it appears likelythat activation of the autologous complement by apoptotic cells may promote the processing of apoptotic cell by phagocytes.
2. The effect of complement receptor upon the functions of Fc receptors--Synergistic function between FcR and CR3. We compared the phagocytosis of immune complexes (IC) and iC3b-opsonized derivatives (iC3b-IC) by human neutrophils. The phagocytosis of iC3b-IC was greater than that of IC.The enhanced phagocytosis of iC3b-IC was decreased to the same level to that of IC upon treatment of cells with ethanol, aninhibitor for phospholipase D.The IC phagocytosis was inhibited more effectively by anti-FcR lllB,whereas the iC3b-lC phagocytosis was partly inhibited only by anti-FcRll . These results in dicate that the main FcR might differin IC and iC3b-IC phagocytosis.
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