Human herpesvirus 6 infection impairs Toll-like receptor signaling

被引：22

作者：

Murakami, Yuichi ^{[1
]}

Tanimoto, Kazushi ^{[1
]}

Fujiwara, Hiroshi ^{[1
,2
]}

An, Jun ^{[1
]}

Suemori, Koichiro ^{[1
]}

Ochi, Toshiki ^{[1
]}

Hasegawa, Hitoshi ^{[1
,2
]}

Yasukawa, Masaki ^{[1
,2
]}

机构：

[1] Ehime Univ, Grad Sch Med, Dept Bioregulatory Med, Toon, Ehime 7910295, Japan

[2] Ehime Univ, Proteomed Res Ctr, Toon, Ehime 7910295, Japan

来源：

VIROLOGY JOURNAL | 2010年 / 7卷

关键词：

I-KAPPA-B; TRANSCRIPTIONAL DOWN-REGULATION; DENDRITIC CELLS; IKK-BETA; T-CELLS; HUMAN-HERPESVIRUS-6; KINASE; PHOSPHORYLATION; INHIBITION; ACTIVATION;

D O I：

10.1186/1743-422X-7-91

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Human herpesvirus 6 (HHV-6) has a tropism for immunocompetent cells, including T lymphocytes, monocytes/macrophages, and dendritic cells (DCs) suggesting that HHV-6 infection affects the immunosurveillance system. Tolllike receptor (TLR) system plays an important role in innate immunity against various pathogens. In the present study, we investigated the effect of HHV-6 infection on the expression and intracellular signaling of TLRs in DCs. Although expression levels of TLRs were not decreased or slightly elevated following HHV-6 infection, the amounts of cytokines produced following stimulation with ligands for TLRs appeared to be dramatically decreased in HHV-6-infected DCs as compared to mock-infected DCs. Similarly, phosphorylation levels of TAK-1, I kappa B kinase, and I kappa B-a following stimulation of HHV-6-infected DCs with lipopolysaccharide, which is the ligand for TLR4, appeared to be decreased. These data show that HHV-6 impairs intracellular signaling through TLRs indicating the novel mechanism of HHV-6-mediated immunomodulation.

引用

页数：5

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