登革热病毒抑制原代人树突状细胞Ⅰ型干扰素的产生。
Dengue virus inhibits the production of type I interferon in primary human dendritic cells.
机构信息
Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1124, New York, NY 10029, USA.
出版信息
J Virol. 2010 May;84(9):4845-50. doi: 10.1128/JVI.02514-09. Epub 2010 Feb 17.
Abstract
Dengue virus (DENV) infects human immune cells in vitro and likely infects dendritic cells (DCs) in vivo. DENV-2 productive infection induces activation and release of high levels of chemokines and proinflammatory cytokines in monocyte-derived DCs (moDCs), with the notable exception of alpha/beta interferon (IFN-alpha/beta). Interestingly, DENV-2-infected moDCs fail to prime T cells, most likely due to the lack of IFN-alpha/beta released by moDCs, since this effect was reversed by addition of exogenous IFN-beta. Together, our data show that inhibition of IFN-alpha/beta production by DENV in primary human moDCs is a novel mechanism of immune evasion.
摘要
登革热病毒（DENV）在体外感染人类免疫细胞，并且可能在体内感染树突状细胞（DC）。DENV-2 生产性感染诱导单核细胞衍生的树突状细胞（moDC）中高水平趋化因子和促炎细胞因子的激活和释放，干扰素-α/β（IFN-α/β）是一个显著的例外。有趣的是，DENV-2 感染的 moDC 不能刺激 T 细胞，这很可能是由于 moDC 释放的 IFN-α/β 缺乏，因为通过添加外源性 IFN-β 可以逆转这种效应。总之，我们的数据表明，DENV 在原代人 moDC 中抑制 IFN-α/β 的产生是一种新的免疫逃避机制。
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