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2015 Fiscal Year Final Research Report

The Mechanism of Glycan-dependent Cytotoxicity by NK cells

Research Project

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Project/Area Number 25460702
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Laboratory medicine
Research InstitutionToho 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
KeywordsNK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.

Free Research Field

病態生化学

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Published: 2017-05-10  

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