The Mechanism of Glycan-dependent Cytotoxicity by NK cells
| Project/Area Number |
25460702
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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 |
Laboratory medicine
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| Research Institution | Toho University |
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Principal Investigator |
HIGAI Koji 東邦大学, 薬学部, 准教授 (70297711)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | NK細胞 / 糖鎖依存性細胞傷害 / NCRs / NKG2s / CD94 / NKG2D / NKG2A / NCR / IL-2 / 局在化 / 転写制御 |
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| Outline of Final Research Achievements |
In this study, we identified a transcriptional start sites and its promoter structure of CD94, NKG2D and NCR2. The effects of IL-2 treatment for the Glycan-dependent cytotoxicity on NK cells was studied:
(1) Expression of NKG2A was decreased on KHYG cells-treated with IL-2. (2) The CD94-NKG2A complexes did not colocalized with GM1 at the cell membrane in KHYG cells-treated with IL-2.
This study suggests that the NKG2D signals was enhanced by the inhibition of signal transduction from NKG2A by glycan ligand in NK cells with IL-2, resulting that the glycan-dependent cytotoxicity was induced.
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Report
(4 results)
Research Products
(3 results)
