Role of T helper 17-mediated immune responses in the pathogenesis of refractory asthma.
| Project/Area Number |
21790783
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 閉塞性肺疾患 / 気管支喘息 / サイトカイン |
|---|
| Research Abstract |
Neutrophilic inflammation and Th17-type immune responses are characteristics of airway inflammation in severe asthma. Dopamine D1-like receptor(D1-like-R) antagonist suppresses Th17 differentiation. In this study, we clarified that D1-like-R antagonist significantly suppressed ovalbumin(OVA)-induced neutrophilic airway inflammation. It also inhibited the production of IL-17 and infiltration of Th17 cells in the lung. Further, it suppressed the production of IL-23 by lung CD11c+antigen-presenting cells. These findings suggest the possibility that antagonizing D1-like-R serves as a promising new strategy for controlling neutrophil-dominant severe asthma.
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Report
(4 results)
Research Products
(39 results)
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[Journal Article] Dopamine D1-Like Receptor Antagonist Attenuates Th17-Mediated Immune Response and Ovalbumin Antigen-Induced Neutrophilic Airway Inflammation2011
Author(s)
Nakagome K, Imamura M, Okada H, Kawahata K, Inoue T, Hashimoto K, Harada H, Higashi T, Takagi R, Nakano K, Hagiwara K, Kanazawa M, Dohi M, Nagata M, Matsushita S
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Journal Title
J Immunol
Volume: 186
Pages: 5975-5982
Related Report
Peer Reviewed
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