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首页> 外文期刊>Vaccine >Infection of mouse bone marrow-derived dendritic cells by live attenuated Japanese encephalitis virus induces cells maturation and triggers T cells activation.
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Infection of mouse bone marrow-derived dendritic cells by live attenuated Japanese encephalitis virus induces cells maturation and triggers T cells activation.

机译:减毒活日本脑炎病毒感染小鼠骨髓来源的树突状细胞可诱导细胞成熟并触发T细胞活化。

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An attenuated Japanese encephalitis virus (JEV) strain SA14-14-2, generated from the wild strain SA14, is an effective live vaccine against JEV infection. It has led to a significant decrease in JEV infection around the world. Although it is highly effective, the mechanism for its robust immunity was not well investigated. In this study, the interaction of SA14-14-2 with bone marrow-derived dendritic cells (bmDCs) was investigated. Our results showed that the infection of bmDCs with SA14-14-2 resulted in viral replication and upregulation of bmDC maturation marker molecules (CD40, CD80, CD83 and MHC I). SA14-14-2 infection also stimulated the production of interferon- alpha (IFN- alpha ), monocyte chemoattractant protein-1 (MCP-1/CCL2), tumor necrosis factor- alpha (TNF- alpha ) and interleukin-6 (IL-6) of bmDC. Both MLR and ELISPOT assay showed an enhanced allostimulatory capacity of SA14-14-2-infected bmDCs. Furthermore, the SA14-14-2-infected bmDCs impaired the expansion of Foxp3+ regulatory T (Treg) cells with immunosuppressive potential, suggesting that SA14-14-2 infection induced antiviral immunity rather than immunosuppression. Taken together, our results indicated that SA14-14-2 infection caused bmDC maturation, changed the expression profiles of several cytokines, and triggered T cell activation. This offered an insight in the immunologic mechanisms associated with the high efficiency of the SA14-14-2 vaccine.
机译:由野生株SA14产生的减毒日本脑炎病毒(JEV)株SA14-14-2是抗JEV感染的有效活疫苗。它已导致全世界JEV感染的显着减少。尽管它非常有效,但对其鲁棒性免疫的机制尚未进行充分研究。在这项研究中,研究了SA14-14-2与骨髓来源的树突状细胞(bmDCs)的相互作用。我们的结果表明,SA14-14-2感染bmDCs导致病毒复制和bmDC成熟标记分子(CD40,CD80,CD83和MHC I)上调。 SA14-14-2感染还刺激了干扰素-α(IFN-α),单核细胞趋化蛋白1(MCP-1 / CCL2),肿瘤坏死因子-α(TNF-α)和白介素6(IL- 6)的bmDC。 MLR和ELISPOT分析均显示SA14-14-2感染的bmDC的同种异体刺激能力增强。此外,感染SA14-14-2的bmDC损害具有免疫抑制潜能的Foxp3 +调节性T(Treg)细胞的扩增,表明SA14-14-2感染诱导了抗病毒免疫而不是免疫抑制。综上所述,我们的结果表明SA14-14-2感染导致bmDC成熟,改变了几种细胞因子的表达谱,并触发了T细胞活化。这提供了与SA14-14-2疫苗高效相关的免疫机制的见解。

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