| Project/Area Number |
23659496
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Chiba University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | メモリーTh2 細胞 / 気管支喘息 / 肺血管リモデリング / IL-25 / Th2細胞 / メモリーTh2細胞 / シグナルシークエンストラップ法 / DNAマイクロアレイ |
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| Research Abstract |
The characteristics of asthma are mainly mediated by antigen-specific memory Th2 cells and their cytokines including IL-4, IL-5, and IL-13. In this study, we tried to identify cell surface molecules specific for memory Th2 cells by using DNA microarray analysis and retrovirus-mediated signal sequence trap screening. However, unfortunately, we could not identify memory Th2 cell-specific molecules within this research period. On the other hand, we found that prolonged Th2-type immune inflammation in the lung induces the expression of IL-25 and pulmonary arterial remodeling (PAR). Injection of anti-IL-25 antibody inhibited antigen-induced PAR. Lung-specificIL-25 transgenic mice (CC10 IL-25 mice) but not CC10 IL-25 NKT^<-/-> mice spontaneouslydeveloped PAR. These results suggest that prolonged expression of IL-25 in the lung induces PARby NKT cell-dependent mechanisms.
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