2013 Fiscal Year Final Research Report
Elucidation of oncogenic role of novel EBV latent genes
| Project/Area Number |
23590534
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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 |
Virology
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| Research Institution | Shimane University (2013)
Hokkaido University (2011-2012) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
JINUSHI Masahisa 北海道大学, 遺伝子病制御研究所, 准教授 (40318085)
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| Co-Investigator(Renkei-kenkyūsha) |
NANBO Asuka 北海道大学, 医学部, 准教授 (60359487)
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| Project Period (FY) |
2011 – 2013
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| Keywords | EBウイルス / 病原性 / 腫瘍 |
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| Research Abstract |
EBV is a ubiquitous human herpes virus with oncogenic activity. Around 10 latent genes are known and many of them play roles for development and maintenance of EBV-associated malignancies. Recently identified BNLF2a gene was expressed at an early lytic infection and contributed evasion of EBV-infected cells from specific CD8+ T cell recognition. Here, we found BNLF2a and novel BNLF2b, of which gene locates 9-bp downstream of BNLF2a gene, were expressed not only at lytic, but at latent infection. Since BNLF2a downregulated surface MHC class I, BNLF2a may contribute establishment of persistently EBV infected B cells in vivo by inducing immune evasion from viral antigen-specific CD8+ T cell recognition. BNLF2b conferred apoptotic resistance to EBV-infected cells, thus supporting proliferation of infected cells. Suggesting that both BNLF2a and BNLF2b contribute to development of EBV-associated malignancies through proliferation of EBV-infected cells.
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[Journal Article] TIM-4 glycoprotein-mediated degradation of dying tumor cells by autophagy leads to reduced antigen presentation and increased immune tolerance2013
Author(s)
Baghdadi M, Yoneda A, Yamashina T, Nagao H, Komohara Y, Nagai S, Akiba H, Foretz M, Yoshiyama H, Kinoshita I, Dosaka-Akita H, Takeya M, Viollet B, Yagita H, Jinushi M
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Journal Title
Immunity
Volume: 39
Pages: 1070-1081
DOI
Peer Reviewed
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[Journal Article] Dendritic cell-derived TIM-3 is a universal repressor of nucleic acids-mediated antitumor innate immune responses2012
Author(s)
Chiba S, Baghdadi M, Akiba H, Kinoshita I, Yoshiyama H, Hirashima M, Dosaka-Akita H, Uede T, Takaoka A, Yagita H, Jinushi M
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Journal Title
Nat Immunol
Volume: 13
Pages: 832–842
Peer Reviewed
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