Basic study in the role of C-type lectin receptors to develop novel regulating system of acute respiratory distress syndrome caused by influenza infection.
| Project/Area Number |
18K16510
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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 55060:Emergency medicine-related
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| Research Institution | Niigata University |
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Principal Investigator |
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | インフルエンザ / C型レクチン受容体 / 急性呼吸促迫症候群 |
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| Outline of Final Research Achievements |
The function of C-type lectin receptors (CLRs), known as pathogen-derived carbohydrate recognition receptors, in influenza infection has not been fully understood. Inflammatory cytokine production by bone marrow-derived dendritic cells upon stimulation with various types of influenza virus hemagglutinin (HA) was significantly reduced in Dectin-2 knockout mice compared to wild type mice. This reduction was closely related to the interaction between HA including high mannose polysaccharide and Dectin-2. The present studies suggested that Dectin-2 may play an important role for regulating severe influenza pneumoniae such as acute respiratory distress syndrome.
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| Academic Significance and Societal Importance of the Research Achievements |
これまでの研究では、宿主によるインフルエンザウイルス認識機構へのCLRsの関与については報告されていた一方で、インフルエンザ感染による宿主免疫応答におけるCLRsの役割については理解が進んでいなかった。本研究結果は、Dectin-2を欠損した状態下では炎症反応誘導が抑制されるという重要な学術的知見が得られ、Dectin-2が炎症制御の鍵となることが分かった。今後、過剰免疫応答に関与する免疫系細胞や炎症性メディエーターの動態が明らかになれば、Dectin-2を標的とした過剰炎症抑制を目指した治療薬の開発などに応用可能であり、社会的意義は非常に大きい。
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Report
(3 results)
Research Products
(2 results)
