Elucidation of new molecular mechanism targeting at overcoming individual difference of postoperative rejection in liver transplant patients
| Project/Area Number |
16K18946
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Medical pharmacy
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Research Collaborator |
MASUDA Satohiro
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 免疫抑制薬 / 移植 / 個別化医療 / 肝移植 / バイオマーカー / 薬理 / 免疫抑制剤 |
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| Outline of Final Research Achievements |
In this study, with the aim of establishing a higher quality postoperative immunosuppressive therapy, it is newly viewed as a candidate factor（Immunomodulatory factors of hepatitis C reactio
n and rejection :IFR） related to individual differences in rejection expression in patients who underwent liver transplantation for liver disease caused by hepatitis C virus. By analyzing the effect of donor liver constitution (difference in IFR gene expression) on liver transplantation in recipients, I examined that differences in IFR expression level and types can be used as biomarkers for predicting rejection after liver transplantation.
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| Academic Significance and Societal Importance of the Research Achievements |
肝移植における急性拒絶反応には細胞障害性T細胞（CTL）とNK細胞が中心的な役割を果たしている。NK様培養細胞株KHYG-1と白血病細胞株k562を利用したkilling assay系を利用して、組み替えIFRを添加することにより、KHYG-1細胞の細胞障害活性が低下するかどうかを指標にIFRの細胞障害活性への影響を評価した。IFR存在下ではKHYG-1細胞の細胞障害活性は低下し、k562細胞の細胞死が回避される傾向にあることを確認した。一方でラットモデルを用いた検討ではTh1細胞、制御性T細胞（Treg細胞）に及ぼすIFRの影響はほとんどないことが示された。
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Report
(4 results)
Research Products
(14 results)
