2017 Fiscal Year Final Research Report
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 |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| 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 |
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| 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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| Free Research Field |
ウイルス学
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