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Human B-cell proliferation is also driven by ligands of Toll-like receptors (TLRs), notably viral or bacterial DNA containing unmethylated CpG dinucleotides, which triggers TLR9. Here we quantitatively investigated how TLR stimuli influence EBV-driven B-cell proliferation and expression of effector molecules. CpG DNA synergistically increased EBV-driven proliferation and transformation, T-cell costimulatory molecules, and early production of interleukin-6. CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-mediated transformation of both memory and naive B cells. Ligands for TLR2 or TLR7\/8 or whole bacteria had a weaker but still superadditive effect on B-cell transformation. Additionally, CpG DNA facilitated the release of transforming virus by established EBV-infected lymphoblastoid cell lines. These results suggest that the proliferation of EBV-infected B cells and their capability to interact with immune effector cells may be directly influenced by components of bacteria or other microbes present at the site of infection.<\/jats:p>","DOI":"10.1128\/jvi.01400-09","type":"journal-article","created":{"date-parts":[[2010,1,21]],"date-time":"2010-01-21T02:09:21Z","timestamp":1264039761000},"page":"3612-3623","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":50,"title":["Toll-Like Receptor Agonists Synergistically Increase Proliferation and Activation of B Cells by Epstein-Barr Virus"],"prefix":"10.1128","volume":"84","author":[{"given":"Stefanie","family":"Iskra","sequence":"first","affiliation":[{"name":"Department of Gene Vectors, Helmholtz-Zentrum Mu\u0308nchen, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Kalla","sequence":"additional","affiliation":[{"name":"Department of Gene Vectors, Helmholtz-Zentrum Mu\u0308nchen, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henri-Jacques","family":"Delecluse","sequence":"additional","affiliation":[{"name":"Department of Virus-Associated Tumors, German Cancer Research Center, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Hammerschmidt","sequence":"additional","affiliation":[{"name":"Department of Gene Vectors, Helmholtz-Zentrum Mu\u0308nchen, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Moosmann","sequence":"additional","affiliation":[{"name":"Department of Gene Vectors, Helmholtz-Zentrum Mu\u0308nchen, Munich, Germany"},{"name":"Clinical Cooperative Group Molecular Oncology, Helmholtz-Zentrum Mu\u0308nchen, and Ludwig-Maximilians-Universita\u0308t, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.02227-07"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.182.2.851"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.200366597"},{"key":"e_1_3_2_5_2","doi-asserted-by":"crossref","first-page":"4045","DOI":"10.4049\/jimmunol.158.9.4045","volume":"158","year":"1997","unstructured":"Beatty, P. 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