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诱导病毒感染细胞凋亡及随后的吞噬作用作为一种抗病毒机制。

Induction of Apoptosis and Subsequent Phagocytosis of Virus-Infected Cells As an Antiviral Mechanism.

作者信息

Nainu Firzan, Shiratsuchi Akiko, Nakanishi Yoshinobu

机构信息

Laboratory of Pharmacology and Toxicology, Faculty of Pharmacy, Hasanuddin University, Makassar, Indonesia.

Laboratory of Host Defense and Responses, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.

出版信息

Front Immunol. 2017 Sep 28;8:1220. doi: 10.3389/fimmu.2017.01220. eCollection 2017.

DOI:10.3389/fimmu.2017.01220
PMID:29033939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5624992/
Abstract

Viruses are infectious entities that hijack host replication machineries to produce their progeny, resulting, in most cases, in disease and, sometimes, in death in infected host organisms. Hosts are equipped with an array of defense mechanisms that span from innate to adaptive as well as from humoral to cellular immune responses. We previously demonstrated that mouse cells underwent apoptosis in response to influenza virus infection. These apoptotic, virus-infected cells were then targeted for engulfment by macrophages and neutrophils. We more recently reported similar findings in the fruit fly , which lacks adaptive immunity, after an infection with C virus. In these experiments, the inhibition of phagocytosis led to severe influenza pathologies in mice and early death in . Therefore, the induction of apoptosis and subsequent phagocytosis of virus-infected cells appear to be an antiviral innate immune mechanism that is conserved among multicellular organisms. We herein discuss the underlying mechanisms and significance of the apoptosis-dependent phagocytosis of virus-infected cells. Investigations on the molecular and cellular features responsible for this underrepresented virus-host interaction may provide a promising avenue for the discovery of novel substances that are targeted in medical treatments against virus-induced intractable diseases.

摘要

病毒是传染性实体,它们劫持宿主的复制机制来产生后代,在大多数情况下会导致疾病,有时还会导致受感染宿主生物体死亡。宿主具备一系列防御机制,涵盖从先天免疫到适应性免疫,以及从体液免疫到细胞免疫反应。我们之前证明,小鼠细胞在受到流感病毒感染时会发生凋亡。这些发生凋亡的、被病毒感染的细胞随后会被巨噬细胞和中性粒细胞吞噬。我们最近在缺乏适应性免疫的果蝇感染C病毒后也报道了类似的发现。在这些实验中,吞噬作用的抑制导致小鼠出现严重的流感病理症状并过早死亡。因此,诱导病毒感染细胞凋亡并随后进行吞噬似乎是一种在多细胞生物中保守的抗病毒先天免疫机制。我们在此讨论病毒感染细胞依赖凋亡的吞噬作用的潜在机制和意义。对这种未被充分研究的病毒 - 宿主相互作用的分子和细胞特征进行研究,可能为发现针对病毒引起的难治性疾病的医学治疗靶点的新物质提供一条有前景的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/b929b24e682e/fimmu-08-01220-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/8e079fc58e12/fimmu-08-01220-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/bd1ebc23e3d2/fimmu-08-01220-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/30170db1a816/fimmu-08-01220-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/b929b24e682e/fimmu-08-01220-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/8e079fc58e12/fimmu-08-01220-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/ae39aa939274/fimmu-08-01220-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/f5234b587ea0/fimmu-08-01220-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/ba58e6018754/fimmu-08-01220-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/bd1ebc23e3d2/fimmu-08-01220-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/30170db1a816/fimmu-08-01220-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cde3/5624992/b929b24e682e/fimmu-08-01220-g007.jpg

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