| pubmed-article:17609264 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17609264 | lifeskim:mentions | umls-concept:C0014644 | lld:lifeskim |
| pubmed-article:17609264 | lifeskim:mentions | umls-concept:C0947647 | lld:lifeskim |
| pubmed-article:17609264 | lifeskim:mentions | umls-concept:C2247737 | lld:lifeskim |
| pubmed-article:17609264 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:17609264 | pubmed:dateCreated | 2007-8-30 | lld:pubmed |
| pubmed-article:17609264 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:17609264 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17609264 | pubmed:citationSubset | IM | lld:pubmed |
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