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J Virol. 2010 Apr;84(7):3612-23. doi: 10.1128/JVI.01400-09. Epub 2010 Jan 20.

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

Author information

  • 1Helmholtz-Zentrum München, Marchioninistr. 25, 81377 Munich, Germany.

Abstract

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.

PMID:
20089650
[PubMed - indexed for MEDLINE]
PMCID:
PMC2838115
Free PMC Article

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