Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1124, New York, NY 10029, USA.
J Virol. 2010 May;84(9):4845-50. doi: 10.1128/JVI.02514-09. Epub 2010 Feb 17.
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.
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。