Enterovirus 71 Infection of Human Dendritic Cells
Enterovirus 71 Infection of Human Dendritic Cells
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DOI：
10.3181/0903-rm-116
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发表时间：
2009-10-01
影响因子：
3.2
通讯作者：
Chen, Shun-Hua
中科院分区：
文献类型：
--
作者：
Lin, Yu-Wen;Wang, Shainn-Wei;Chen, Shun-Hua
肠病毒71型（EV71）可导致数十万幼儿死亡和长期神经系统后遗症，但其发病机制尚不清楚。树突状细胞（dc）在抗病毒免疫中起着至关重要的作用，它作为专业的抗原呈递细胞向初始T细胞呈递，并通过分泌细胞因子来调节免疫反应。本研究表明，EV71可有效感染人未成熟dc，并在dc中表达病毒抗原。DC-SIGN部分介导EV71进入dc。进一步的分析表明，EV71增加了dc中细胞因子、白细胞介素-6、白细胞介素-12和肿瘤坏死因子-a的活力、活化和释放。此外，EV71使dc能够刺激t细胞增殖。总之，这些发现表明EV71在体内感染人类dc很可能引发保护性免疫，因为在受感染的小鼠中，T细胞和IL-6都具有降低死亡率的功能。中国生物医学工程学报（英文版），2009
Enterovirus 71 (EV71) causes death and long-term neurologic sequelae in hundreds of thousands of young children, but its pathogenesis remains elusive. Dendritic cells (DCs) play a crucial role in antiviral immunity by functioning as professional antigen-presenting cells to prime T cells and by secreting cytokines to modulate immune responses. Here, we show that EV71 productively infected human immature DCs and expressed viral antigen in DCs. EV71 entry into DCs was partially mediated by DC-SIGN. Further analyses revealed that EV71 increased the viability, activation, release of cytokines, interleukin-6, interleukin-12, and tumor necrosis factor-a in DCs. Moreover, EV71 enabled DCs to stimulate T-cell proliferation. Collectively, these findings suggest that EV71 infection of human DCs in vivo is very likely to elicit protective immunity, because in infected mice, both T cells and IL-6 function to reduce mortality. Exp Biol Med 234:1166-1173, 2009