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

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.

journal_name

J Virol

journal_title

Journal of virology

authors

Iskra S,Kalla M,Delecluse HJ,Hammerschmidt W,Moosmann A

doi

10.1128/JVI.01400-09

subject

Has Abstract

pub_date

2010-04-01 00:00:00

pages

3612-23

issue

7

eissn

0022-538X

issn

1098-5514

pii

JVI.01400-09

journal_volume

84

pub_type

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