2014 Fiscal Year Final Research Report
Kinetics of fetal-antigen specific cytotoxic T cell (CTL) and protection role of placenta for feto-maternal tolerance
| Project/Area Number |
24592487
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAKESHITA Toshiyuki 日本医科大学, 医学部, 教授 (60188175)
NEGISHI Yasuyuki 日本医科大学, 医学部, 助教 (50644580)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 生殖免疫 / 妊娠 / B7-H1(PD-L1) / 胎児抗原特異的CTL / 自然免疫 / 樹状細胞 |
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| Outline of Final Research Achievements |
We have investigated the mechanism of fetal-antigen specific cytotoxic T cell (CTL) for feto-maternal tolerance focused on the B7-H1 (PD-L1). B7-H1 is expressed on placenta and several kinds of tissues. B7-H1 is the suppressive co-stimulatory molecule and is thought to suppress CTL activity. In this study, fetal-antigen specific CTL was induced by the induction of anti-B7-H1 antibody and the 41-BB, co-stimulatory molecule, for pregnant mice in vivo CTL assay. However, the miscarriage was not facilitated by these treatments. PD-L1 is expressed not only the placenta but also dendritic cells and macrophages, and PD-1 is expressed not only T cells but also NK cells. From these points of view, the correlation between the PD-L1 molecules and innate immunity were investigated for the murine pregnancy. We found the new strategy of miscarriage concerned with the innate immunity including the kinetics of PD-L1 molecules.
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| Free Research Field |
産婦人科学
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