2014 Fiscal Year Final Research Report
Role of natural killer T cells in chronic inflammation of atherogenesis
| Project/Area Number |
23591096
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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 |
Circulatory organs internal medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Hiroyuki 北海道大学, 大学院医学研究科, 教授 (70264017)
KINUGAWA Shintaro 北海道大学, 大学院医学研究科, 講師 (60399871)
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| Research Collaborator |
TOKUHARA Satoshi 北見赤十字病院, 循環器内科, 副部長
SAITO Akimichi 北海道大学, 大学病院, 医員 (40735502)
NISHIKAWA Mikito 帯広協会病院, 循環器内科, 医長
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Keywords | 慢性炎症 / 動脈硬化 / マクロファージ / リンパ球 / 免疫調節 |
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| Outline of Final Research Achievements |
The purpose of this study was to elucidate the role of natural killer T (NKT) cells in chronic inflammation elicited by dyslipidemia, which result in atherosclerosis. Splenocytes from apolipoprotein-E deficient mice, including mononuclear phagocytes and NKT cells, were cultured with α-Galactosylceramide (α-GalCer), which specifically activates NKT cells, and significantly reduced in the production of inflammatory cytokines compared to those from wild-type mice, suggesting NKT cell anergy. Splenocytes cultured with Th1 or Th2 cytokines were stimulated with α-GalCer, but did not differ in the production of inflammatory cytokines between apolipoprotein-E deficient mice and wild-type mice. Thus, we could not elucidate the significant role of NKT cells in chronic inflammation in the present study.
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| Free Research Field |
循環器病学
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