Elucidation of glycosylation-dependent influenza virus recognition mechanism by novel innate immune receptor
| Project/Area Number |
16K09585
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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 |
Respiratory organ internal medicine
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| Research Institution | Kitasato University |
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Principal Investigator |
UEMATSU Takayuki 北里大学, 北里大学メディカルセンター, 上級研究員 (90414060)
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| Research Collaborator |
IIZASA Ei-ichi
HARA HHiromitsu
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | インフルエンザウイルス / 自然免疫 / 感染症 / シグナル伝達 / 免疫学 / ウイルス |
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| Outline of Final Research Achievements |
Previous studies have revealed that IgSFR2, a novel innate immune receptor, recognizes the hemagglutinin (HA) of influenza virus (IFV) in a glycosylation-dependent manner. Therefore, carbohydrate motifs derived from HA recognized by IgSFR2 were chemically synthesized, and in vitro and in vivo effects were examined. As a result, administration of carbohydrate motifs reduced the entry of IFV into cells by competitively inhibiting the mechanism of IFV adsorption or uptake via IgSFR2 in host cells. Furthermore, it has been shown that the survival rate of IFV-infected mice is improved because the amount of inflammatory cytokines/chemokines produced from host cells is suppressed.
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| Academic Significance and Societal Importance of the Research Achievements |
今後、IFV感染モデルマウスに対するIgSFR2リガンド投与の免疫学的作用を詳細に検討することにより、IFV感染症の重篤例にみられるインフルエンザ肺炎の新たな治療アプローチを開発することができると期待される。また、今後の研究により、IgSFR2を介したHA依存的な宿主細胞へのIFV吸着・侵入機構などの生理的な意義が解明された場合には、HAワクチン副反応の効果的な予測やHAワクチン効果増強への応用も期待される。
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Report
(4 results)
Research Products
(19 results)
