首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >The dual-specific binding of dengue virus and target cells for the antibody-dependent enhancement of dengue virus infection.
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The dual-specific binding of dengue virus and target cells for the antibody-dependent enhancement of dengue virus infection.

机译:登革热病毒和靶细胞的双重特异性结合,以抗体依赖性方式增强登革热病毒感染。

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摘要

Using flow cytometric assay and monoclonal anti-dengue Ab, we observed that both anti-E and anti-prM Abs could enhance dengue virus infection in a concentration-dependent but serotype-independent manner. Increases were found in both the percentage of dengue-infected cells and the expression of dengue E and NS1 protein per cell. Dengue virion binding and infection were enhanced on FcR-bearing cells via the Fc-FcgammaRII pathway. Furthermore, anti-prM Ab also enhanced dengue virion binding and infection on cells lacking FcR, such as BHK-21 or A549 cells, by the mechanism of peptide (CPFLKQNEPEDIDCW)-specific binding. Anti-prM Ab cross-reacted with BHK-21 or A549 cells and recognized self-Ags such as heat shock protein 60. In summary, a novel mechanism of anti-prM Ab-mediated enhancement on dengue virus infection was found to be mediated by dual specific binding to dengue virion and to target cells, in addition to the traditional enhancement on FcR-bearing cells.
机译:使用流式细胞仪和单克隆抗登革热抗体,我们观察到抗E和抗prM Abs均可以浓度依赖性但不依赖血清型的方式增强登革热病毒感染。登革热感染细胞的百分比以及每个细胞中登革热E和NS1蛋白的表达均增加。登革病毒粒子的结合和感染通过Fc-FcgRmII途径在带有FcR的细胞上得到增强。此外,抗prM Ab还通过肽(CPFLKQNEPEDIDCW)特异性结合的机制,增强了登革病毒粒子对缺乏FcR的细胞(如BHK-21或A549细胞)的结合和感染。抗prM Ab与BHK-21或A549细胞交叉反应,并识别自身抗原,例如热休克蛋白60。总而言之,发现抗prM Ab介导的登革热病毒感染增强的新机制是通过以下途径介导的除了对带有FcR的细胞的传统增强作用外,还与登革热病毒颗粒和靶细胞具有双重特异性结合。

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