| Project/Area Number |
15590639
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Mie University |
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Principal Investigator |
MURATA Kazumoto Mie University, University Hospital, Research Associate, 医学部附属病院, 助手 (40345971)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRAKI Katsuya Mie University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (90263003)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | NKT cells / NK cells / CD1d receptor / adenovirus / B型肝炎ウイルス / アデノウイルス / マウス |
|---|
| Research Abstract |
Five days after intravenous injection of adenovirus expressing HBV (adeno-HBV) to BALB/c mice, serum HBsAg showed a peak whereas no elevation in adeno-GFP (control virus) injected mice during follow-up. The number of intrahepatic lymphocytes increased 1 day after injection in mice injected either adeno-HBV or adeno-GFP, suggesting that this effect is due to adenovirus itself. Howevr, 5 days after injection, the number of NK cells increased again whereas no increase in adeno-GFP injected mice. The number of CD1d tertramer positive cells decreased 1 day after injection by both adenovirus. The number of CD1d tetramer positive cells recovered in a few days in adeno-GFP injected mice. In contrast, it was not recovered until 10 days after injection of adeno-HBV. NK cytotoxicity using Yac-1 cells was up-regulated 1 day after injection of both virus. Then, it gradually went back to normal in adeno-GFP injected mice whereas iNK cytotoxicity up-regulated again in adeno-HBV injected mice. From the differences on Day 5 after injection, HBV may decrease the number of CD1d tetramer positive cells and increase the number of NK cells. Injection of adeno-HBV to GD1 knockout mice demonstrated the disappearance of NK cytotoxicity. These results may indicate that HBV up-regulated NK cells through NKT cells activation.
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