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Human Plasmacytoid Dendritic Cells Elicited Different Responses after Infection with Pathogenic and Nonpathogenic Junin Virus Strains.人类浆细胞样树突状细胞在感染致病性和非致病性胡宁病毒株后引发了不同反应。
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Junin Virus Triggers Macrophage Activation and Modulates Polarization According to Viral Strain Pathogenicity.胡宁病毒根据病毒株的致病性触发巨噬细胞激活并调节极化。
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Highly Pathogenic New World Arenavirus Infection Activates the Pattern Recognition Receptor Protein Kinase R without Attenuating Virus Replication in Human Cells.高致病性新大陆沙粒病毒感染激活模式识别受体蛋白激酶R但不减弱其在人细胞中的病毒复制
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本文引用的文献

1
The Z proteins of pathogenic but not nonpathogenic arenaviruses inhibit RIG-I-like receptor-dependent interferon production.致病性沙粒病毒而非非致病性沙粒病毒的Z蛋白会抑制视黄酸诱导基因I样受体依赖性干扰素的产生。
J Virol. 2015 Mar;89(5):2944-55. doi: 10.1128/JVI.03349-14. Epub 2014 Dec 31.
2
RIG-I enhanced interferon independent apoptosis upon Junin virus infection.在胡宁病毒感染后,RIG-I增强了不依赖干扰素的细胞凋亡。
PLoS One. 2014 Jun 11;9(6):e99610. doi: 10.1371/journal.pone.0099610. eCollection 2014.
3
Type I interferons protect T cells against NK cell attack mediated by the activating receptor NCR1.I 型干扰素通过激活受体 NCR1 保护 T 细胞免受 NK 细胞的攻击。
Immunity. 2014 Jun 19;40(6):961-73. doi: 10.1016/j.immuni.2014.05.003. Epub 2014 Jun 5.
4
Type I interferon protects antiviral CD8+ T cells from NK cell cytotoxicity.Ⅰ型干扰素保护抗病毒 CD8+T 细胞免受 NK 细胞的细胞毒性。
Immunity. 2014 Jun 19;40(6):949-60. doi: 10.1016/j.immuni.2014.05.004. Epub 2014 Jun 5.
5
Potent inhibition of Junín virus infection by interferon in murine cells.干扰素对鼠细胞中胡宁病毒感染的强烈抑制作用。
PLoS Negl Trop Dis. 2014 Jun 5;8(6):e2933. doi: 10.1371/journal.pntd.0002933. eCollection 2014 Jun.
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A novel mitochondrial MAVS/Caspase-8 platform links RNA virus-induced innate antiviral signaling to Bax/Bak-independent apoptosis.一种新型的线粒体 MAVS/Caspase-8 平台将 RNA 病毒诱导的先天抗病毒信号与 Bax/Bak 非依赖性细胞凋亡联系起来。
J Immunol. 2014 Feb 1;192(3):1171-83. doi: 10.4049/jimmunol.1300842. Epub 2014 Jan 3.
7
Human plasmacytoid dendritic cells: from molecules to intercellular communication network.人类浆细胞样树突状细胞:从分子到细胞间通讯网络。
Front Immunol. 2013 Nov 12;4:372. doi: 10.3389/fimmu.2013.00372. eCollection 2013.
8
The MyD88 pathway in plasmacytoid and CD4+ dendritic cells primarily triggers type I IFN production against measles virus in a mouse infection model.浆细胞样树突状细胞和 CD4+树突状细胞中的 MyD88 通路主要在小鼠感染模型中针对麻疹病毒引发 I 型 IFN 的产生。
J Immunol. 2013 Nov 1;191(9):4740-7. doi: 10.4049/jimmunol.1301744. Epub 2013 Sep 27.
9
Innate immune response to arenaviral infection: a focus on the highly pathogenic New World hemorrhagic arenaviruses.天然免疫对沙粒病毒感染的应答:关注高致病性新域出血沙粒病毒。
J Mol Biol. 2013 Dec 13;425(24):4893-903. doi: 10.1016/j.jmb.2013.09.028. Epub 2013 Sep 26.
10
Paramyxovirus activation and inhibition of innate immune responses.副黏液病毒激活与固有免疫反应抑制。
J Mol Biol. 2013 Dec 13;425(24):4872-92. doi: 10.1016/j.jmb.2013.09.015. Epub 2013 Sep 20.

人类浆细胞样树突状细胞在感染致病性和非致病性胡宁病毒株后引发了不同反应。

Human Plasmacytoid Dendritic Cells Elicited Different Responses after Infection with Pathogenic and Nonpathogenic Junin Virus Strains.

作者信息

Negrotto Soledad, Mena Hebe A, Ure Agustin E, Jaquenod De Giusti Carolina, Bollati-Fogolín Mariela, Vermeulen Elba M, Schattner Mirta, Gómez Ricardo M

机构信息

Instituto de Medicina Experimental, CONICET-Academia Nacional de Medicina, Buenos Aires, Argentina.

Instituto de Biotecnología y Biología Molecular, CONICET-Universidad Nacional de La Plata, La Plata, Argentina.

出版信息

J Virol. 2015 Jul;89(14):7409-13. doi: 10.1128/JVI.01014-15. Epub 2015 Apr 29.

DOI:10.1128/JVI.01014-15
PMID:25926646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4473584/
Abstract

The arenavirus Junin virus (JUNV) is the etiologic agent of Argentine hemorrhagic fever. We characterized the JUNV infection of human peripheral blood-derived plasmacytoid dendritic cells (hpDC), demonstrating that hpDC are susceptible to infection with the C#1 strain (attenuated) and even more susceptible to infection with the P (virulent) JUNV strain. However, hpDC elicited different responses in terms of viability, activation, maturation, and cytokine expression after infection with both JUNV strains.

摘要

沙粒病毒胡宁病毒(JUNV)是阿根廷出血热的病原体。我们对人外周血来源的浆细胞样树突状细胞(hpDC)的JUNV感染进行了表征,证明hpDC易受C#1株(减毒株)感染,甚至更易受P(毒株)JUNV株感染。然而,在用两种JUNV毒株感染后,hpDC在活力、激活、成熟和细胞因子表达方面引发了不同的反应。