Inhibitory mechanisms of NK92 cell cytotoxicity by IL-17 stimulation

Persistent ID (NDL): info:ndljp/pid/12071562

Material type: 博士論文

Author: 足立, 哲也

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Publication date: 2018-03-29

Material Format: Digital

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Name of awarding university/degree: 大阪歯科大学,博士（歯学）

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Note (General)：: We investigated mechanisms of intracellular signaling on IL-17 stimulated NK92 cells. We confirmed that the majority of NK92 cells expressed IL-17RA. ...

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Material Type: 博士論文
Title: Inhibitory mechanisms of NK92 cell cytotoxicity by IL-17 stimulation
Author/Editor: 足立, 哲也
Author Heading: 足立, 哲也
Publication Date: 2018-03-29
Publication Date (W3CDTF): 2018-03-29
Alternative Title: IL-17 による NK92 細胞の細胞傷害能抑制機構について
Degree grantor/type: 大阪歯科大学
Date Granted: 2018-03-29
Date Granted (W3CDTF): 2018-03-29
Dissertation Number: 乙第1609号
Degree Type: 博士（歯学）
Conferring No. (Dissertation): 乙第1609号
Text Language Code: eng
Subject Heading: IL-17｜NK cells｜cytotoxicity
Target Audience: 一般
Note (General): We investigated mechanisms of intracellular signaling on IL-17 stimulated NK92 cells. We confirmed that the majority of NK92 cells expressed IL-17RA. The phosphorylation of ERK and JNK were not altered in the absence or presence of IL-17. Phosphorylation of p38 was observed in the absence of IL-17, but its phosphorylation was suppressed in the presence of IL-17. There was slight phosphorylation of GSK3-β in the absence of IL-17, which was increased in the presence of IL-17. These results suggest that p38 and GSK3-β may be involved in suppressing the cytotoxicity of IL-17 stimulated NK92 cells.
2017年度
Persistent ID (NDL): info:ndljp/pid/12071562
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Collection: 障害者向け資料
Collection (Materials For Handicapped People:1): テキストデータ
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
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Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2022-02-06T04:33:19+09:00
Date Created (W3CDTF): 2018-05-18
Format (IMT): application/pdf
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Periodical Title (URI): http://id.nii.ac.jp/1392/00000177/
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