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Epstein-Barr virus (EBV)-encoded small RNA is released from EBV-infected cells and activates signaling from toll-like receptor 3

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Title: Epstein-Barr virus (EBV)-encoded small RNA is released from EBV-infected cells and activates signaling from toll-like receptor 3
Authors: Iwakiri, Dai Browse this author
Zhou, Li Browse this author
Samanta, Mrinal Browse this author
Matsumoto, Misako Browse this author →KAKEN DB
Ebihara, Takashi Browse this author
Seya, Tsukasa Browse this author →KAKEN DB
Imai, Shosuke Browse this author
Fujieda, Mikiya Browse this author
Kawa, Keisei Browse this author
Takada, Kenzo Browse this author
Issue Date: 28-Sep-2009
Publisher: Rockefeller University Press
Journal Title: Journal of Experimental Medicine
Volume: 206
Issue: 10
Start Page: 2091
End Page: 2099
Publisher DOI: 10.1084/jem.20081761
Abstract: Epstein-Barr virus-encoded small RNA (EBER) is nonpolyadenylated, noncoding RNA that forms stem-loop structure by intermolecular base-pairing, giving rise to double-stranded RNA (dsRNA)-like molecules, and exists abundantly in EBV-infected cells. Here, we report that EBER induces signaling from the Toll-like receptor 3 (TLR3), which is a sensor of viral double-stranded RNA (dsRNA) and induces type I IFN and proinflammatory cytokines. A substantial amount of EBER, which was sufficient to induce signaling from TLR3, was released from EBV-infected cells, and the majority of the released EBER existed as a complex with a cellular EBER-binding protein La, suggesting that EBER was released from the cells by active secretion of La. Sera from patients with infectious mononucleosis (IM), chronic active EBV infection (CAEBV), and EBV-associated hemophagocytic lymphohistiocytosis (EBV-HLH), whose general symptoms are caused by proinflammatory cytokines contained EBER, and addition of RNA purified from the sera into culture medium induced signaling from TLR3 in EBV-transformed lymphocytes and peripheral mononuclear cells. Furthermore, DCs treated with EBER showed mature phenotype and antigen presentation capacity. These findings suggest that EBER, which is released from EBV-infected cells, is responsible for immune activation by EBV, inducing type I IFN and proinflammatory cytokines. EBER-induced activation of innate immunity would account for immunopathologic diseases caused by active EBV infection.
Rights: © 2009 Iwakiri et al.
Type: article
URI: http://hdl.handle.net/2115/39542
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 高田 賢藏

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