| Project/Area Number |
15K09796
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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 |
Dermatology
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
Imai Yasutomo 兵庫医科大学, 医学部, 講師 (10529514)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMANISHI Kiyofumi 兵庫医科大学, 医学部, 教授 (10182586)
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| Research Collaborator |
JITSUKAWA Orie 兵庫医科大学, 医学部, 実験補助
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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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ILC2 / IL-33 / ２型自然リンパ球 / アトピー性皮膚炎 / 自然リンパ球 |
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| Outline of Final Research Achievements |
Interleukin-33 (IL-33) stimulates group 2 innate lymphoid cells (ILC2). We generated a transgenic mouse expressing IL-33 driven by a keratin-14 promoter (IL33Tg) and showed that IL-33 elicits atopic dermatitis (AD)-like inflammation with activation of ILC2 (Imai Y, PNAS, 2013; Imai Y, Sci Rep, 2017). When bone marrow from ILC2-lacking, RORα-deficient mice was transplanted into IL33Tg mice, the development of AD-like dermatitis was completely suppressed, and ILC2-derived cytokines/chemokines such as IL-5, IL-13, CCL5 and CCL11 were significantly reduced in the skin. These results suggest that IL-33-induced dermatitis is ILC2 dependent.
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