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J Infect Dis. 2023 Nov 13;228(Suppl 7):S582-S586. doi: 10.1093/infdis/jiad377.
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本文引用的文献

1
Epidemiology of Ebolaviruses from an Etiological Perspective.从病因学角度看埃博拉病毒的流行病学
Pathogens. 2023 Feb 3;12(2):248. doi: 10.3390/pathogens12020248.
2
Tumor necrosis factor is a necroptosis-associated alarmin.肿瘤坏死因子是一种与坏死性凋亡相关的警报素。
Front Immunol. 2022 Dec 12;13:1074440. doi: 10.3389/fimmu.2022.1074440. eCollection 2022.
3
IL-18R-mediated HSC quiescence and MLKL-dependent cell death limit hematopoiesis during infection-induced shock.IL-18R 介导体细胞静止和 MLKL 依赖性细胞死亡限制感染诱导性休克期间的造血。
Stem Cell Reports. 2021 Dec 14;16(12):2887-2899. doi: 10.1016/j.stemcr.2021.10.011. Epub 2021 Nov 18.
4
Necroptosis, pyroptosis and apoptosis: an intricate game of cell death.细胞程序性死亡方式:细胞坏死、细胞焦亡与细胞凋亡。
Cell Mol Immunol. 2021 May;18(5):1106-1121. doi: 10.1038/s41423-020-00630-3. Epub 2021 Mar 30.
5
Ebola virus-mediated T-lymphocyte depletion is the result of an abortive infection.埃博拉病毒介导的 T 淋巴细胞耗竭是感染失败的结果。
PLoS Pathog. 2019 Oct 24;15(10):e1008068. doi: 10.1371/journal.ppat.1008068. eCollection 2019 Oct.
6
RIP1/RIP3-regulated necroptosis as a target for multifaceted disease therapy (Review).RIP1/RIP3 调节的坏死性凋亡作为多方面疾病治疗的靶点(综述)。
Int J Mol Med. 2019 Sep;44(3):771-786. doi: 10.3892/ijmm.2019.4244. Epub 2019 Jun 14.
7
Ebola Virus Shed Glycoprotein Triggers Differentiation, Infection, and Death of Monocytes Through Toll-Like Receptor 4 Activation.埃博拉病毒脱落糖蛋白通过 Toll 样受体 4 激活触发单核细胞分化、感染和死亡。
J Infect Dis. 2018 Nov 22;218(suppl_5):S327-S334. doi: 10.1093/infdis/jiy406.
8
The Induction of IL-1β Secretion Through the NLRP3 Inflammasome During Ebola Virus Infection.埃博拉病毒感染过程中通过 NLRP3 炎性小体诱导白细胞介素-1β 的分泌。
J Infect Dis. 2018 Nov 22;218(suppl_5):S504-S507. doi: 10.1093/infdis/jiy433.
9
Ebola Virus Binding to Tim-1 on T Lymphocytes Induces a Cytokine Storm.埃博拉病毒与 T 淋巴细胞上的 Tim-1 结合会引发细胞因子风暴。
mBio. 2017 Sep 26;8(5):e00845-17. doi: 10.1128/mBio.00845-17.
10
Ebola virus glycoprotein directly triggers T lymphocyte death despite of the lack of infection.尽管没有感染,但埃博拉病毒糖蛋白直接引发T淋巴细胞死亡。
PLoS Pathog. 2017 May 22;13(5):e1006397. doi: 10.1371/journal.ppat.1006397. eCollection 2017 May.

埃博拉病毒与免疫细胞的相互作用通过多种机制导致其死亡。

Interplay of Ebola Virus With Immune Cells Leading to Their Death by Diverse Mechanisms.

机构信息

Department of Pathology.

Galveston National Laboratory, The University of Texas Medical Branch, Galveston.

出版信息

J Infect Dis. 2023 Nov 13;228(Suppl 7):S582-S586. doi: 10.1093/infdis/jiad377.

DOI:10.1093/infdis/jiad377
PMID:37654044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10651200/
Abstract

Inflammation and cytopenia are commonly observed during Ebola virus (EBOV) infection; however, mechanisms responsible for EBOV-induced cell death remain obscure. While apoptosis and necrosis are already identified as mechanisms of cell death induced by the virus, our study demonstrates that THP-1 monocytes and SupT1 T cells exposed to EBOV undergo pyroptosis and necroptosis, respectively, through a direct contact with EBOV, and also mediate pyroptosis or necroptosis of uninfected bystander cells via indirect effects associated with secreted soluble factors. These results emphasize novel aspects of interactions between EBOV and immune cell populations and provide a better understanding of the immunopathogenesis of EBOV disease.

摘要

在埃博拉病毒(EBOV)感染过程中,炎症和细胞减少症很常见;然而,导致 EBOV 诱导的细胞死亡的机制尚不清楚。虽然凋亡和坏死已被确定为病毒诱导的细胞死亡的机制,但我们的研究表明,与 EBOV 直接接触的 THP-1 单核细胞和 SupT1 T 细胞分别经历细胞焦亡和坏死,并且还通过与分泌的可溶性因子相关的间接作用介导未感染旁观者细胞的细胞焦亡或坏死。这些结果强调了 EBOV 和免疫细胞群体之间相互作用的新方面,并更好地理解了 EBOV 疾病的免疫发病机制。