Human herpesvirus 6 infection impairs Toll-like receptor signaling
Human herpesvirus 6 infection impairs Toll-like receptor signaling
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DOI：
10.1186/1743-422x-7-91
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发表时间：
2010-05-10
期刊：
影响因子：
4.8
通讯作者：
Yasukawa, Masaki
中科院分区：
文献类型：
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作者：
Murakami, Yuichi;Tanimoto, Kazushi;Yasukawa, Masaki
人疱疹病毒6型（HHV-6）对免疫能力细胞具有亲和性，包括T淋巴细胞、单核/巨噬细胞和树突状细胞（dc），这表明HHV-6感染影响免疫监视系统。toll样受体（TLR）系统在机体对抗多种病原体的先天免疫中起着重要作用。在本研究中，我们研究了HHV-6感染对dc中TLRs表达和细胞内信号传导的影响。虽然TLRs的表达水平在HHV-6感染后没有降低或略有升高，但与模拟感染的dc相比，HHV-6感染的dc中TLRs配体刺激后产生的细胞因子的数量似乎显著降低。同样，在TLR4配体脂多糖刺激hhv -6感染的dc后，TAK-1、I kappa B激酶和I kappa B-a的磷酸化水平似乎降低。这些数据表明HHV-6通过TLRs破坏细胞内信号通路，提示HHV-6介导的免疫调节新机制。
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.