Suppression of NF-κB and AP-1 activation in monocytic cells persistently infected with measles virus
Suppression of NF-κB and AP-1 activation in monocytic cells persistently infected with measles virus
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DOI：
10.1016/j.virol.2006.11.002
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发表时间：
2007-05-10
期刊：
影响因子：
3.7
通讯作者：
Fujii, Nobuhiro
中科院分区：
文献类型：
--
作者：
Indoh, Tomokazu;Yokota, Shin-ichi;Fujii, Nobuhiro
与麻疹感染相关的高发病率和死亡率的一个主要原因是病毒介导的免疫抑制。在这份报告中，我们提出了一种新的麻疹病毒免疫抑制策略的证据。在麻疹病毒持续感染的人单核细胞系中，我们观察到脂多糖（LPS）诱导的IL-8、RANTES、TNF-α和IL-6产生以及NF-κ B活化的显著抑制。在持续感染麻疹病毒的人上皮细胞系中未观察到这种效应。与未感染的细胞相比，麻疹病毒感染的单核细胞中Toll样受体（TLR）及其相关分子或NF-κ B信号通路的其他细胞内信号分子的表达水平无显著差异。感染的单核细胞表现出LPS诱导的NF-κ B的DNA结合和JNK的磷酸化减少，即转录因子NF-κ B和AP-1的活化。NF-κ B B在麻疹病毒持续感染的人上皮细胞中被组成性激活，LPS处理导致进一步激活。NF-κ B激活的细胞类型特异性抑制代表了麻疹病毒通过感染细胞中诱导的免疫沉默逃离宿主免疫系统的潜在策略。(c)2006年爱思唯尔公司版权所有© 2016
A major cause of the high morbidity and mortality associated with measles infection is attributed to virus-mediated immunosuppression. In this report, we present evidence for a novel strategy of immunosuppression by the measles virus. We observed a marked suppression of lipopolysaccharide (LPS)-induced IL-8, RANTES, TNF-alpha and IL-6 production and NF-kappa B activation in human monocytic cell lines persistently infected with measles virus. This effect was not observed in human epithelial cells lines persistently infected with measles virus. There were no significant differences in expression levels of Toll-like receptors (TLRs) and their associated molecules, or other intracellular signaling molecules of the NF-kappa B signaling pathway in measles-virus-infected monocytic cells compared to uninfected cells. Infected monocytic cells exhibited decreased LPS-induced DNA binding of NF-kappa B and phosphorylation of JNK, namely activation of transcription factors NF-kappa B and AP-1. NF-kappa B was constitutively activated in human epithelial cells persistently infected with measles virus, and LPS treatment resulted in further activation. The cell-type-specific suppression of NF-kappa B activation represents a potential strategy of escape from the host immune system by measles virus via induced immunological silencing in infected cells. (c) 2006 Elsevier Inc. All rights reserved,