Cited 104 times in
Manipulation of the Toll-Like Receptor 7 Signaling Pathway by Epstein-Barr Virus
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이재면 | - |
dc.date.accessioned | 2014-12-21T16:59:11Z | - |
dc.date.available | 2014-12-21T16:59:11Z | - |
dc.date.issued | 2007 | - |
dc.identifier.issn | 0022-538X | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/96725 | - |
dc.description.abstract | Epstein-Barr virus (EBV) infection of primary B cells causes B-cell activation and proliferation. Activation of B cells requires binding of antigen to the B-cell receptor and a survival signal from ligand-bound CD40, signals that are provided by the EBV LMP1 and LMP2A latency proteins. Recently, Toll-like receptor (TLR) signaling has been reported to provide a third B-cell activation stimulus. The interaction between the EBV and TLR pathways was therefore investigated. Both UV-inactivated and untreated EBV upregulated the expression of TLR7 and downregulated the expression of TLR9 in naive B cells. UV-inactivated virus transiently stimulated naive B-cell proliferation in the presence of the TLR7 ligand R837, while addition of the TLR7 antagonist IRS 661 impaired cell growth induced by untreated EBV. Interferon regulatory factor 5 (IRF-5) is a downstream mediator of TLR7 signaling. IRF-5 was induced following EBV infection, and IRF-5 was expressed in B-cell lines with type III latency. Expression of IRF-5 in this setting is surprising since IRF-5 has tumor suppressor and antiviral properties. B-cell proliferation assays provided evidence that EBV modulates TLR7 signaling responses. Examination of IRF-5 transcripts identified a novel splice variant, V12, that was induced by EBV infection, was constitutively nuclear, and acted as a dominant negative form in IRF-5 reporter assays. IRF-4 negatively regulates IRF-5 activation, and IRF-4 was also present in type III latently infected cells. EBV therefore initially uses TLR7 signaling to enhance B-cell proliferation and subsequently modifies the pathway to regulate IRF-5 activity. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 9748~9758 | - |
dc.relation.isPartOf | JOURNAL OF VIROLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adjuvants, Immunologic/pharmacology | - |
dc.subject.MESH | Alternative Splicing/drug effects | - |
dc.subject.MESH | Alternative Splicing/genetics | - |
dc.subject.MESH | Alternative Splicing/physiology | - |
dc.subject.MESH | Aminoquinolines/pharmacology | - |
dc.subject.MESH | B-Lymphocytes/metabolism* | - |
dc.subject.MESH | B-Lymphocytes/virology | - |
dc.subject.MESH | CD40 Antigens/genetics | - |
dc.subject.MESH | CD40 Antigens/metabolism | - |
dc.subject.MESH | CD40 Ligand/genetics | - |
dc.subject.MESH | CD40 Ligand/metabolism | - |
dc.subject.MESH | Cell Line, Transformed | - |
dc.subject.MESH | Cell Proliferation/radiation effects | - |
dc.subject.MESH | Cell Survival/drug effects | - |
dc.subject.MESH | Cell Survival/genetics | - |
dc.subject.MESH | Cell Survival/radiation effects | - |
dc.subject.MESH | Epstein-Barr Virus Infections/genetics | - |
dc.subject.MESH | Epstein-Barr Virus Infections/metabolism* | - |
dc.subject.MESH | Gene Expression Regulation/drug effects | - |
dc.subject.MESH | Gene Expression Regulation/genetics | - |
dc.subject.MESH | Gene Expression Regulation/radiation effects | - |
dc.subject.MESH | HeLa Cells | - |
dc.subject.MESH | Herpesvirus 4, Human/genetics | - |
dc.subject.MESH | Herpesvirus 4, Human/metabolism* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Imiquimod | - |
dc.subject.MESH | Interferon Regulatory Factors/genetics | - |
dc.subject.MESH | Interferon Regulatory Factors/metabolism | - |
dc.subject.MESH | Lymphocyte Activation*/drug effects | - |
dc.subject.MESH | Lymphocyte Activation*/genetics | - |
dc.subject.MESH | Lymphocyte Activation*/radiation effects | - |
dc.subject.MESH | Signal Transduction*/drug effects | - |
dc.subject.MESH | Signal Transduction*/genetics | - |
dc.subject.MESH | Signal Transduction*/radiation effects | - |
dc.subject.MESH | Toll-Like Receptor 7/agonists | - |
dc.subject.MESH | Toll-Like Receptor 7/metabolism* | - |
dc.subject.MESH | Toll-Like Receptor 9/genetics | - |
dc.subject.MESH | Toll-Like Receptor 9/metabolism | - |
dc.subject.MESH | Ultraviolet Rays | - |
dc.subject.MESH | Viral Matrix Proteins/genetics | - |
dc.subject.MESH | Viral Matrix Proteins/metabolism | - |
dc.subject.MESH | Virus Latency/drug effects | - |
dc.subject.MESH | Virus Latency/genetics | - |
dc.subject.MESH | Virus Latency/radiation effects | - |
dc.title | Manipulation of the Toll-Like Receptor 7 Signaling Pathway by Epstein-Barr Virus | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Microbiology (미생물학) | - |
dc.contributor.googleauthor | Heather J. Martin | - |
dc.contributor.googleauthor | Jae Myun Lee | - |
dc.contributor.googleauthor | S. Diane Hayward | - |
dc.contributor.googleauthor | Dermot Walls | - |
dc.identifier.doi | 10.1128/JVI.01122-07 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03071 | - |
dc.relation.journalcode | J01930 | - |
dc.identifier.eissn | 1098-5514 | - |
dc.identifier.pmid | 17609264 | - |
dc.contributor.alternativeName | Lee, Jae Myun | - |
dc.contributor.affiliatedAuthor | Lee, Jae Myun | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 81 | - |
dc.citation.number | 18 | - |
dc.citation.startPage | 9748 | - |
dc.citation.endPage | 9758 | - |
dc.identifier.bibliographicCitation | JOURNAL OF VIROLOGY, Vol.81(18) : 9748-9758, 2007 | - |
dc.identifier.rimsid | 36432 | - |
dc.type.rims | ART | - |
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