Epstein-Barr virus infection-induced inflammasome activation in human leukocytes.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19638
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pediatrics
• Research Institution: Nagoya University
• Principal Investigator: TORII Yuka 名古屋大学, 医学系研究科, 特別研究員(RPD) (00770281)
• Research Collaborator: KAWADA Junichi ; MURATA Takayuki
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: Epstein-Barr virus / Inflammasomes / interleukin-1β

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.

Free Research Field

感染症