| Project/Area Number |
26670236
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
Kawai Taro 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (50456935)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 自然免疫 / シグナル伝達 / 細胞死 / アジュバント / ウイルス核酸 / 樹状細胞 / ウイルス / 獲得免疫 / サイトカイン / 炎症 |
|---|
| Outline of Final Research Achievements |
Pathogen infection triggers death of host cells, but its role in regulation of immune responses remains unclear. In this study, we examined whether cell death of murine dendritic cells is induced by stimulation with agonists for innate immune receptors, and found that treatment of dendritic cells with R837, an agonist for Toll-like receptor (TLR) 7, resulted in cell death among other TLR agonists tested. Furthermore, this cell death was independent on TLR7, suggesting that R837 induces cell death via unknown pathways. As R837 is known as an adjuvant for virus infection, these results suggest that endogenous molecules released by dying dendritic cells upon R837 stimulation play roles in shaping adaptive immunity to viruses.
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