NDV entry into dendritic cells through macropinocytosis and suppression of T lymphocyte proliferation

文献类型： 外文期刊

第一作者： Tan, Lei

作者： Tan, Lei;Zhang, Yuqiang;Qiao, Changtao;Yuan, Yanmei;Sun, Yingjie;Qiu, Xusheng;Meng, Chunchun;Song, Cuiping;Liao, Ying;Ding, Chan;Munir, Muhammad;Nair, Venugopal;Ding, Zhuang;Liu, Xiufan;Ding, Chan

作者机构：

关键词： Newcastle disease virus; Dendritic cells; Macropinocytosis; Apoptosis; T lymphocyte proliferation

期刊名称：VIROLOGY （ 影响因子：3.616； 五年影响因子：3.967 ）

ISSN： 0042-6822

年卷期： 2018 年 518 卷

页码：

收录情况： SCI

摘要： Newcastle disease virus (NDV) causes major economic losses in the poultry industry. Previous studies have shown that NDV utilizes different pathways to infect various cells, including dendritic cells (DCs). Here, we demonstrate that NDV gains entry into DCs mainly via macropinocytosis and clathrin-mediated endocytosis. The detection of cytokines interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-12 (IL-12), interleukin-4 (IL-4) and interleukin-10 (IL-10) indicates that NDV significantly induces Th1 responses and lowers Th2 responses. Furthermore, NDV entry into DCs resulted in the upregulation of TNF-related apoptosis-inducing ligand (TRAIL) and cleaved caspase-3 proteins, which in turn activated the extrinsic apoptosis pathway and induced DCs apoptosis. Transwell (R) co-culture demonstrated that direct contact between live NDV-stimulated DCs and T cells, rather than heated-inactivated NDV, inhibited CD4(+) T cell proliferation. Taken together, these findings provide new insights into the mechanism underlying NDV infections, particularly in relation to antigen presentation cells and suppression of T cell proliferation.

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