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Enterovirus 71 2C Protein Inhibits TNF-α–Mediated Activation of NF-κB by Suppressing IκB Kinase β Phosphorylation

IκB激酶 磷酸化 促炎细胞因子 αBκ NF-κB 小干扰RNA 信号转导 NFKB1型 肿瘤坏死因子α 激酶 生物 细胞生物学 免疫沉淀 分子生物学 癌症研究 炎症 转录因子 免疫学 生物化学 转染 基因
作者
Zhenhua Zheng,Hongxia Li,Zhenfeng Zhang,Jin Meng,Da Mao,Bingke Bai,Baojing Lu,Panyong Mao,Qinxue Hu,Hanzhong Wang
出处
期刊:Journal of Immunology [American Association of Immunologists]
卷期号:187 (5): 2202-2212 被引量:87
标识
DOI:10.4049/jimmunol.1100285
摘要

Abstract Enterovirus 71 (EV71), a single, positive-stranded RNA virus, has been regarded as the most important neurotropic enterovirus after the eradication of the poliovirus. EV71 infection can cause hand, foot, and mouth disease or herpangina. Cytokine storm with elevated levels of proinflammatory and inflammatory cytokines, including TNF-α, has been proposed to explain the pathogenesis of EV71-induced disease. TNF-α–mediated NF-κB signaling pathway plays a key role in inflammatory response. We hypothesized that EV71 might also moderate host inflammation by interfering with this pathway. In this study, we tested this hypothesis and identified EV71 2C protein as an antagonist of TNF-α–mediated activation of NF-κB signaling pathway. Expression of 2C protein significantly reduced TNF-α–mediated NF-κB activation in 293T cells as measured by gene reporter and gel mobility shift assays. Furthermore, overexpression of TNFR-associated factor 2-, MEK kinase 1-, IκB kinase (IKK)α-, or IKKβ-induced NF-κB activation, but not constitutively active mutant of IKKβ (IKKβ SS/EE)-induced NF-κB activation, was inhibited by 2C protein. These data together suggested that the activation of IKKβ is most likely targeted by 2C; this notion was further strengthened by immunoblot detection of IKKβ phosphorylation and IκBα phosphorylation and degradation. Coimmunoprecipitation and colocalization of 2C and IKKβ expressed in mammalian cells provided compelling evidence that 2C interacts with IKKβ. Collectively, our data indicate that EV71 2C protein inhibits IKKβ activation and thus blocks NF-κB activation.

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