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流感病毒感染的树突状细胞免疫调节机制 被引量:2

Study on dendritic cell immune regulation mechanism of influenza virus infection
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摘要 目的揭示流感病毒感染导致重症化肺炎的树突细胞免疫调控机制。方法 6~8周龄C57BL/6小鼠构建对照组(VEH)、扎那米韦处理组(Z)和扎那米韦、塞来昔布和美沙拉秦联合处理组(Z+C+M)的实验动物模型,流式细胞分析树突状细胞免疫提呈能力和T细胞的免疫能力;ELISA方法分析促炎性细胞因子水平。结果在流感病毒感染后4 d和6 d,Z+C+M组的MHC Class I、MHC Class II、CD80和CD86荧光强度表达量显著低于VEH组和Z组(P<0.05);Z+C+M组的CD4+T细胞和CD8+T细胞数量显著低于VEH组和Z组(P<0.05);Z+C+M组的促炎性细胞因子IL-1β,TNF-α和IL-6水平显著低于VEH组和Z组(P<0.05)。结论树突状细胞抗原提呈能力的强弱对流感病毒感染重症化肺炎的形成起着非常重要的作用。 Objective To reveal the dendritic cell immune regulation mechanism of influenza virus infection in severe pneumonia. Methods Six to eight weeks of C57BL/6 mice were the control group (VEH), zanamivir treatment group (Z) and zanamivir,celecoxib and salad qin combined treatment group (Z+C+M) were experimental animal models. Flow cytometry analysis was used to test dendritic cell immune ability and T cell immune;ELISA method was to analyze the promotion of inflammatory cytokine levels. Results After influenza virus infection,4 d and 6 d,Z+C+M group of MHC Class I, MHC Class II, CD80 and CD86 fluorescence intensity expression was significantly lower than that of VEH and Z group (P〈0. 05) ;Z+C+M group of CIMT cells and CD8 T cells was significantly lower than that of VEH and Z group (P〈0. 05) ;Z+C+M group of inflammatory cytokines IL-1 beta,TNF alpha and IL-6 were significandy lower than that of VEH and Z group (P〈0. 05). Conclusion The strength of the promotion of dendritic cell antigen presenting ability is very important in the formation of severe pneumonia of influenza virus infection.
出处 《公共卫生与预防医学》 2014年第3期11-15,共5页 Journal of Public Health and Preventive Medicine
基金 延安大学高水平大学学科建设基础医学项目(2013 SXTS02)
关键词 流感病毒 细胞因子风暴 树突细胞 免疫调控 Influenza virus Cytokine storm Dendritic cells Immune regulation
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