| Project/Area Number |
15K09692
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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 |
Pediatrics
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| Research Institution | Kyushu University |
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Principal Investigator |
Tanaka Tamami 九州大学, 医学研究院, 学術研究員 (60423547)
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| Co-Investigator(Kenkyū-buntansha) |
西尾 壽乘 九州大学, 大学病院, 助教 (00507783)
神野 俊介 九州大学, 大学病院, 助教 (60725919)
本村 良知 九州大学, 大学病院, 助教 (10737175)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 川崎病 / 自然免疫 / 血管炎 |
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| Outline of Final Research Achievements |
We found that CD11c(+)MHC class II(+) cells accumulated in the heart of FK565-treated mice before arteritis development. Morphological features and gene expression signatures of the cardiac CD11c(+)MHC class II(+) cells suggested that this population is closely related to macrophages, and thus, we designated them cardiac CD11c(+) macrophages. Nod1 in nonhematopoietic cells was required for the increase of cardiac CD11c(+) macrophages and arteritis development. Among them, cardiac endothelial cells produced a large amount of chemokines in response to FK565. Endothelial cell-specific blockade of Nod1 signaling suppressed FK565-induced expression of these chemokines, accumulation of cardiac CD11c(+) macrophages, and subsequent coronary arteritis development.
These results suggest that cardiac CD11c(+) macrophages play a pivotal role in the pathogenesis of acute coronary arteritis.
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