| Project/Area Number |
26460108
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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 |
Pharmacology in pharmacy
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| Research Institution | Setsunan University |
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Principal Investigator |
Nabe Takeshi 摂南大学, 薬学部, 教授 (40228078)
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| Co-Investigator(Kenkyū-buntansha) |
福井 裕行 徳島大学, 大学院医歯薬学研究部(薬学系), 特任教授 (90112052)
水谷 暢明 神戸薬科大学, 薬学部, 准教授 (90340447)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | IL-33 / 喘息 / アトピー / 制御性T細胞 / 抗アレルギー薬 |
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| Outline of Final Research Achievements |
In the pathogenesis of intractable asthma, IL-33 has been known to be a key molecule bridging between the innate and acquired immune systems. In this study, we analyzed mechanisms underlying IL-33 production, and immunopharmacological modulation of IL-33. Allergic IL-33 production induced by an intratracheal antigen challenge in sensitized mice was mediated by neither mast cells nor Th2 cells. The administered antigen formed an immune complex with the antigen-specific IgG antibody, followed by incorporation into the alveolar macrophages through the cellular suface FcgRII/III, leading to the IL-33 production in the lung. The IL-33 production was sensitive to steroid anti-inflammatory drug treatment. On the other hand, as a new method for regulation of allergy, adoptive transfer of in vitro-differentiated IL-10-producing T cells effectively suppressed asthmatic responses in mice in vivo.
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