| Project/Area Number |
18K16135
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 54020:Connective tissue disease and allergy-related
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| Research Institution | Hirosaki University |
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Principal Investigator |
Nakano Manabu 弘前大学, 保健学研究科, 助教 (10436016)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 好塩基球 / 細胞外ヌクレオチド / Gタンパク質共役型受容体 / ENTPD / P2Y6 / cAMP |
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| Outline of Final Research Achievements |
We confirmed the effect of P2Y6 receptor signal on IgE-dependent activation of human basophils. Basophils treated with UDP increased cAMP and IP1, but not RhoGTP. Increased expression of CD203c and CD63 on basophils induced by anti-IgE antibody was attenuated by YM-254890, a Gq protein inhibitor. On the other hand, 2',5'-dideoxyadenosine, a cAMP synthase inhibitor, attenuated only the increase in CD63 expression in basophils induced by anti-IgE antibody.
Basophils expressed ecto-nucleotidases and were able to confirm that UTP was hydrolyzed to UDP. POM-1, an extracellular nucleotide hydrolase inhibitor, reduced IgE-dependent activation of human basophils.
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| Academic Significance and Societal Importance of the Research Achievements |
多くの日本国民が花粉症などのⅠ型アレルギー疾患に罹患しているが、治療法の殆どは対処療法であり、根本的な治療法の確立が求められている。現時点で唯一のアレルギーの根本的治療法といえるアレルゲン免疫療法は、重篤な副作用が誘発されることや、使用できるアレルゲンが限定されているなど、課題が残されている。
好塩基球はアレルギー反応で重要な役割を果たしており、その活性化制御はアレルギー疾患の新規治療法の開発につながる。
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