2015 Fiscal Year Final Research Report
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 |
Section | 一般 |
Research Field |
Laboratory medicine
|
Research Institution | Toho University |
Principal Investigator |
HIGAI Koji 東邦大学, 薬学部, 准教授 (70297711)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Keywords | NK細胞 / 糖鎖依存性細胞傷害 / NCRs / NKG2s / CD94 |
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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Free Research Field |
病態生化学
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