| Project/Area Number |
25461492
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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 |
Collagenous pathology/Allergology
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| Research Institution | Chiba University |
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Principal Investigator |
Tamachi Tomohiro 千葉大学, 医学(系)研究科(研究院), 助教 (20456015)
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| Co-Investigator(Kenkyū-buntansha) |
HIROSE Koichi 千葉大学, 大学院医学研究院, 准教授 (90400887)
TAKATORI Hiroaki 千葉大学, 医学部附属病院, 助教 (30568225)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 難治性喘息 / IL-23 / 樹状細胞 / 気道上皮細胞 |
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| Outline of Final Research Achievements |
To elucidate the underlying mechanisms of refractory asthma, our objective was to identify the factor that induces IL-23 production from dendritic cells. We also aimed to clarify the roles of Dectin-2, a C-type lectin receptor for fungal α-mannan, expressed on dendritic cells and the roles of IκBNS expressed in hematopoietic cells in HDM-induced allergic airway inflammation.
We found Dectin-2 expressed on CD11b+ DCs induced IL-23 expression and promoted HDM-induced airway inflammation. We also found CD11b+ DCs isolated from Dectin-2-deficent mice expressed lower levels of proinflammatory cytokines and co-stimulatory molecules which could lead to Th2 and Th17 cell differentiation than those from wild-type mice. In addition, we found HDM-induced airway inflammation was exacerbated in mice lacking IκBNS in hematopoietic cells. We are currently searching for epithelial cell-derived factors that induce IL-23 production from dendritic cells in asthma by a novel co-culture approach.
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