| Project/Area Number |
16K19638
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Nagoya University |
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Principal Investigator |
TORII Yuka 名古屋大学, 医学系研究科, 特別研究員(RPD) (00770281)
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| Research Collaborator |
KAWADA Junichi
MURATA Takayuki
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Epstein-Barr virus / Inflammasomes / interleukin-1β / EBV / インフラマソーム / 単球 / ウイルス / 自然免疫 |
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| Outline of Final Research Achievements |
Inflammasomes are cytoplasmic sensors that regulate the caspase-1 activation and the secretion of interleukin-1β (IL-1β) or interleukin-18 (IL-18) in response to foreign molecules. Inflammasome activation in human leukocytes during Epstein-Barr virus (EBV) infection was investigated. It was shown that EBV could infect not only to B lymphocyte cell lines, but also to T lymphocyte and monocyte cell lines. EBV infection induced caspase-dependent IL-1β production in monocyte cell lines and primary human monocytes, while not in B-cell or T-cell lines. To identify the sensor molecule, we examined the mRNA and the protein levels of NLR family pyrin domain-containing 3 (NLRP3), absent in melanoma 2 (AIM2), and interferon-inducible protein 16 (IFI16). Increased AIM2 levels were observed in EBV-infected monocyte cell lines. Our results suggest that EBV infection of human monocytes induces caspase-1-dependent IL-1β production, and that AIM2 is involved in this response.
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