| Project/Area Number |
63570779
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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 |
Obstetrics and gynecology
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| Research Institution | Osaka University Medical School |
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Principal Investigator |
MATSUZAKI N. Osaka Univ.Dept.Obst Gyn. assistant professor, 医学部, 助手 (30199781)
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| Co-Investigator(Kenkyū-buntansha) |
SAJI F. Osaka Univ.Dept.Obst Gyn. Lecturer, 医学部, 講師 (90093418)
OHASHI K. Osaka Univ.Dept.Obst Gyn. assistant professor, 医学部, 助手 (30203897)
KOYAMA M. Osaka Univ.Dept.Obst Gyn. assistant professor, 医学部, 助手 (00183351)
KAMEDA T. Osaka Univ.Dept.Obst Gyn. assistant professor, 医学部, 助手 (70204641)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1988: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Pregnancy / Immunoregulation / Trophoblast / Maternal T cells / LAK cells / Maternal T cells / 妊娠 / T細胞調節機序 / 胎盤 / 絨毛癌 |
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| Research Abstract |
Fetus is a semiallogeneic graft to mother because of expression of paternal MHC expression. Placenta present between fetomaternal interface regulates maternal immune attacks to the fetus, of which molecular mechanisms is poorly understood. We have shown that placenta produces soluble factors which potentially modulate maternal immune attacks, and reported that choriocarcinoma cell produce a similar immunoregulatory factor. The choriocarcinoma cell-derived factor suppressed IL-2-dependent human T cell responses which are induced by a tumor promotor (TPA) and calcium ionophore (A23187). The factor failed to suppress the expression of CD 25 molecule and inhibit IL-2 production in T cell activation phase, but blocked IL-2-induced proliferation of T cell blasts. The factor also inhibited IL-2- independent T cell proliferation responses induced by 10 nM TPA, but not association-associated reponses. The factors thus, specifically suppressed proliferation-associated responses. We then examined the activity of factor on rIL-2-induced proliferation of mononuclear cells. The factor suppressed the proliferation on Day 4. We also examined the effect of the factor on LAK cell generation. The factor failed to suppress Day 3 LAK cell which generates without DNA synthesis, but inhibited Day 4 LAK cell, suggesting the presence of heterogeneity in the pattern of LAK cell generation. Taken together with the evidence that the factor did not affect NK cell activity, the factor might be involved in the regulation of maternal immune systems by inhibiting the proliferation-associated events for the establishment and maintenance of pregnancy.
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