The mechanism of natural killer cell-mediated recognition against hepatitis virus infection.
Project/Area Number |
15K08498
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Virology
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Research Institution | Okayama University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 肝炎ウイルス / ナチュラルキラー細胞 / 自然免疫応答 / 細胞障害性 / NKG2Dリガンド / NKG2D受容体 / ULBP1 / ヒト不死化肝細胞 / C型肝炎ウイルス / NK細胞 / IFN-gamma / HCV / HBV |
Outline of Final Research Achievements |
In the present study, we demonstrated that hepatitis C virus (HCV) induced the cell surface expression of ULBP1 in human immortalized hepatocyte PH5CH8 cells and human hepatoma HuH-7 cell-derived RSc cells. Interestingly, NK cell line NK-92 induced cytotoxicity and interferon (IFN)-γ mRNA expression and subsequently reduced the levels of HCV RNA replication during the co-culture with HCV-infected RSc cells. We also suggested that NK-92 cells were stimulated by viral dsRNA relaesed from HCV-infected RSc cells and subsequently induced IFN-γ. From these results, we conclude that ULBP1 is a target of the NK cell-mediated innate immune response in HCV-infected human hepatocytes.
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Report
(4 results)
Research Products
(25 results)
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[Presentation] Antimalarial preclinical drugs, N-89 and N-251, overcome various DAAs-resistant HCVs.2015
Author(s)
Ueda Y, Dansako H, Satoh S, Kim HS, Doi H, Wataya Y, Ikeda M, Kato N.
Organizer
22nd International Symposium on Hepatitis C Virus and Related Viruses
Place of Presentation
Strasbourg, France
Year and Date
2015-10-09
Related Report
Int'l Joint Research
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