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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
| 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)
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Submitter: 高田 賢藏
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