| Project/Area Number |
26461184
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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 |
Respiratory organ internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
Hirose Koichi 千葉大学, 大学院医学研究院, 准教授 (90400887)
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| Co-Investigator(Kenkyū-buntansha) |
高取 宏昌 千葉大学, 医学部附属病院, 助教 (30568225)
鈴木 浩太郎 千葉大学, 医学部附属病院, 講師 (90554634)
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| Co-Investigator(Renkei-kenkyūsha) |
SUZUKI KOTARO 千葉大学, 医学部附属病院, 講師 (90554634)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | C型レクチン / Dectin-1 / Dectin-2 / アレルギー性気道炎症 / Th2細胞 / Th17細胞 / CD11b陽性樹状細胞 |
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| Outline of Final Research Achievements |
It is well known that sensitization against fungi is closely associated with severity of asthma, however, the roles of Dectin-1 and Dectin-2, major PRRs for fungi, in HDM-induced allergic airway inflammation remain unclear. In this study, we examined whether Dectin-1 or Dectin-2 is involved in HDM-induced allergic airway inflammation. We found that HDM-induced eosinophil and neutrophil recruitment into the airways was significantly attenuated in Clec7a-/- mice and in Clec4n-/- as compared with that in wild-type (WT) mice. In addition, HDM-induced cytokine production from mediastinum lymph node cells was reduced in HDM-sensitized Clec7a-/- mice and Clec4n-/- mice. Dectin-1 and Dectin-2 were expressed on CD11b+ dendritic cells (DCs), an essential DC subset for the development of allergic inflammation. Taken together, these results suggest that Dectin-1 and Dectin-2expressed on CD11b+ DCs plays a critical role in the induction of HDM-induced allergic airway inflammation.
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