Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
}
TY - JOUR
T1 - NDV entry into dendritic cells through macropinocytosis and suppression of T lymphocyte proliferation
AU - Tan, Lei
AU - Zhang, Yuqiang
AU - Qiao, Changtao
AU - Yuan, Yanmei
AU - Sun, Yingjie
AU - Qiu, Xusheng
AU - Meng, Chunchun
AU - Song, Cuiping
AU - Liao, Ying
AU - Munir, Muhammad
AU - Nair, Venugopal
AU - Ding, Zhuang
AU - Liu, Xiufan
AU - Ding, Chan
N1 - Copyright © 2018 Elsevier Inc. All rights reserved.
PY - 2018/5
Y1 - 2018/5
N2 - 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-γ (IFN-γ), tumor necrosis factor-α (TNF-α), 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® 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.
AB - 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-γ (IFN-γ), tumor necrosis factor-α (TNF-α), 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® 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.
KW - Newcastle disease virus
KW - Dendritic cells
KW - Macropinocytosis
KW - Apoptosis
KW - T lymphocyte proliferation
U2 - 10.1016/j.virol.2018.02.011
DO - 10.1016/j.virol.2018.02.011
M3 - Journal article
C2 - 29481983
VL - 518
SP - 126
EP - 135
JO - Virology
JF - Virology
SN - 0042-6822
ER -