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作 者:胡雅洁 宋杰 汤贝贝 李菁 刘龙丁 王丽春[1] 王晶晶 张莹 和占龙 李琦涵[1]
机构地区:[1]中国医学科学院医学生物学研究所、云南省重大传染病疫苗研发重点实验室,昆明650118
出 处:《中华微生物学和免疫学杂志》2017年第1期34-42,共9页Chinese Journal of Microbiology and Immunology
摘 要:目的探究EV71与CA16对恒河猴CD1c+DC的感染情况,与两者感染后Ⅰ型干扰素(typeⅠ interferon,IFN-Ⅰ)产生通路中及辅助性T细胞(T helper cells,Th)分化过程中相关基因的改变。方法本文通过采用免疫荧光、qRT-PCR、噬斑实验、流式细胞术等方法比较了EV71与CA16感染恒河猴CD1c+DC在不同的时间点内IFN-Ⅰ的产生,病毒载量、病毒滴度、病毒感染量及Th细胞分化相关的转录因子及细胞因子的表达情况。 结果研究结果显示:EV71与CA16均能感染CD1c+DC;EV71感染CD1c+DC后IFN-Ⅰ产生显著性下降,病毒载量、病毒滴度与病毒感染量上升,Th2与滤泡辅助性T细胞(Tfh)相关的转录因子及细胞因子表达显著性上升;而CA16感染CD1c+DC后IFN-Ⅰ产生显著性上升,病毒载量、病毒滴度与病毒感染量下降,Th1与调节性T细胞(Treg)相关的转录因子及细胞因子表达显著性上升。结论这些结果提示EV71与CA16感染CD1c+DC后可能会造成固有免疫应答与适应性免疫应答显著性差异,这些差异可能与两者诱发的差异性临床症状及病理形成相关。ObjectiveTo investigate enterovirus 71 (EV71) and coxsackievirus A16 (CA16) infections in a cell model of CD1c+ DC from rhesus monkey and to analyze the differences in typeⅠ interferon (IFN-Ⅰ) production and T helper cells(Th) differentiation related molecules following infections.MethodsA comparative analysis was performed to analyze differences in IFN-Ⅰ expression, virus copies, plaque forming units (PFUs) of virus, numbers of virus infection, and expression of the transcription factors and cytokines related to the Th differentiation at different time points following EV71 and CA16 infections in CD1c+ DC by using immunofluorescence, qRT-PCR, plaque formation assay and flow cytometry.ResultsEV71 and CA16 could infect CD1c+ DC derived from rhesus monkey. After infecting CD1c+ DC with EV71, the expression of IFN-Ⅰwas significantly decreased; virus copies, PFUs of virus and numbers of virus infection were increased; the expression of transcription factors and cytokines related to Th2 and follicular helper T cells (Tfh) were markedly increased. However, remarkably enhanced expression of IFN-Ⅰ, down-regulated virus copies, PFUs of virus and numbers of virus infection as well as significantly up-regulated expression of transcription factors and cytokines related to Th1 and regulatory T cells (Tregs) were detected following CA16 infection.ConclusionThis study suggests that the differences in innate and adaptive immunity caused by EV71 and CA16 infections in CD1c+ DC might be closely associated with the distinct clinical symptoms and different pathogenesis of HFMD.
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