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甲型流感病毒感染K562细胞会增加其对自然杀伤细胞裂解的敏感性。

Infection of K562 cells with influenza A virus increases their susceptibility to natural killer lysis.

作者信息

Eisenthal A, Marder O, Lifschitz-Mercer B, Skornick Y, Tirosh R, Irlin Y, Avtalion R, Deutsch M

机构信息

Tel-Aviv Sourasky Medical Center, Israel.

出版信息

Pathobiology. 1997;65(6):331-40. doi: 10.1159/000164144.

DOI:10.1159/000164144
PMID:9491852
Abstract

Natural killer (NK) cells play a role in the natural immunity against tumor cells. In the present study, we demonstrate that infection of the NK-sensitive tumor cell line K562 with influenza A virus caused a substantial increase in lysis of up to sevenfold when compared to noninfected cells. Similar to NK cells, IL-2-activated killer cells exhibited higher lytic activity against virus-infected K562 cells. This effect of the virus correlated with the increase in the expression of intracellular adhesion molecule-1 (ICAM-1) on K562 cells. Changes in the susceptibility to NK lysis were accompanied by alterations, within minutes, in the cytoskeleton as detected by intracellular fluorescein fluorescence polarization measured on the Cellscan, a static cytometer. The possible role of iCAM-1 and the cytoskeleton in the cytotoxic response of NK cells is discussed.

摘要

自然杀伤(NK)细胞在针对肿瘤细胞的天然免疫中发挥作用。在本研究中,我们证明,与未感染细胞相比,甲型流感病毒感染NK敏感的肿瘤细胞系K562导致细胞裂解大幅增加,高达七倍。与NK细胞类似,白细胞介素2激活的杀伤细胞对病毒感染的K562细胞表现出更高的裂解活性。病毒的这种作用与K562细胞上细胞间黏附分子1(ICAM-1)表达的增加相关。通过在静态细胞仪Cellscan上测量细胞内荧光素荧光偏振检测到,对NK裂解敏感性的变化在数分钟内伴随着细胞骨架的改变。本文讨论了ICAM-1和细胞骨架在NK细胞细胞毒性反应中的可能作用。

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引用本文的文献

1
Inhibition of human natural killer cell activity by influenza virions and hemagglutinin.流感病毒及其血凝素对人自然杀伤细胞活性的抑制作用。
J Virol. 2010 May;84(9):4148-57. doi: 10.1128/JVI.02340-09. Epub 2010 Feb 17.
2
Depletion of human NK and CD8 cells prior to in vitro H1N1 flu vaccine stimulation increases the number of gamma interferon-secreting cells compared to the initial undepleted population in an ELISPOT assay.在体外进行H1N1流感疫苗刺激之前,对人自然杀伤细胞(NK)和CD8细胞进行耗竭处理,与ELISPOT检测中未进行耗竭处理的初始细胞群体相比,可增加分泌γ干扰素的细胞数量。
Clin Diagn Lab Immunol. 2002 Mar;9(2):230-5. doi: 10.1128/cdli.9.2.230-235.2002.