| Project/Area Number |
25460502
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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 |
Experimental pathology
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Masashi 北里大学, 医学部, 助教 (40611843)
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIMORI Naoki 北海道大学, 病院, 准教授 (70399848)
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| Research Collaborator |
FUJII Satoshi 旭川医科大学, 医学部, 教授 (90291228)
SHIMANO Kentaro
FUJITA Koki
OHISHI Yuhta
HOSHINO Miyuki
Gilfillan Susan Washington Univ
Luc Van Kaer Vanderbilt Univ
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | MAIT細胞 / 動脈硬化症 / NKT細胞 / 動物モデル / 自然T細胞 / アポリポタンパクEノックアウトマウス / 炎症制御 / 生活習慣病 / 病態モデル / マウス / レパトア解析 / マイクロアレイ / 自然リンパ球 / MR1 / CD1d |
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| Outline of Final Research Achievements |
Development of atherosclerosis was ameliorated in NKT cell-deficient mice and aggravated in MAIT cell-deficient apoE knockout (KO) mice. We assumed that a reciprocal regulatory circuit controls the disease process since NKT cells appeared to be activated in MR1-deficient apoE KO mice where the MAIT cells were absent. Although a reciprocal activation of MAIT cells in CD1d-deficient apoE KO mice was not confirmed, we established MR1/CD1d/apoE triple knockout (TKO) mice where both MAIT and NKT cells were dificeint in apoE KO background to test whether the atherosclerotic lesion size either decreased or were similar to the lesion size of MR1-deficient apoE KO mice. In TKO, however, the lseion size was increased compared to the one of MR1/apoE double KO (DKO) mice with the presence of increased NK1.1+ Vβ5+ T cells , suggesting that a minimal regulatory circuit consisted of iNKT and MAIT cells is not sufficient to explain a rather complex process of the development of atherosclerosis.
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