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Iskra, S. ; Kalla, M. ; Delecluse, H.J.* ; Hammerschmidt, W. ; Moosmann, A.

Toll-like receptor agonists synergistically increase proliferation and activation of B cells by Epstein-Barr virus.

J. Virol. 84, 3612-3623 (2010)
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Epstein-Barr virus (EBV) efficiently drives proliferation of human primary B cells in vitro, a process relevant for human diseases such as infectious mononucleosis and posttransplant lymphoproliferative disease. 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.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Human monoclonal-antibodies; Autocrine growth-factor; Infectious-mononucleosis; Anaerobic-bacteria; Signaling pathway; CPG DNA; RIG-I; Expression; EBV; Transformation
ISSN (print) / ISBN 0022-538X
e-ISSN 1098-5514
Journal Journal of Virology
Quellenangaben Volume: 84, Issue: 7, Pages: 3612-3623 Article Number: , Supplement: ,
Publisher American Society for Microbiology (ASM)
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Research Unit Gene Vector (AGV)
CCG Molecular Oncology (AGV-KON)