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嗜酸性粒细胞凋亡:一种新的细胞死亡途径。

ETosis: a novel cell death pathway.

作者信息

Wartha Florian, Henriques-Normark Birgitta

机构信息

Department of Bacteriology, Swedish Institute for Infectious Disease Control, 17182 Solna, Sweden.

出版信息

Sci Signal. 2008 May 27;1(21):pe25. doi: 10.1126/stke.121pe25.

DOI:10.1126/stke.121pe25
PMID:18506034
Abstract

The formation of extracellular traps (ETs) by neutrophils and mast cells is an important mechanism in the innate immune response. These structures consist of a chromatin-DNA backbone with attached antimicrobial peptides and enzymes that trap and kill microbes. After stimulation of neutrophils and mast cells with phorbol esters, chemoattractant peptides, or chemokines, the generation of reactive oxygen species (ROS), such as hydrogen peroxide, by NAPDH [nicotinamide adenine dinucleotide phosphate (reduced form)] oxidase initiates a signaling cascade that leads to the disintegration of the nuclear and cellular membranes and the formation of ETs. This form of cell death is neither apoptotic nor necrotic, but whether it occurs because of the oxidation of phosphatases and kinases, as in other ROS-mediated signaling cascades, remains to be elucidated. These findings implicate "ETosis" as a novel cell death pathway in leukocytes.

摘要

中性粒细胞和肥大细胞形成细胞外陷阱(ETs)是先天免疫反应中的一种重要机制。这些结构由带有附着的抗菌肽和酶的染色质-DNA骨架组成,可捕获并杀死微生物。在用佛波酯、趋化肽或趋化因子刺激中性粒细胞和肥大细胞后,烟酰胺腺嘌呤二核苷酸磷酸(还原型)[NAPDH]氧化酶产生的活性氧(ROS),如过氧化氢,引发信号级联反应,导致核膜和细胞膜解体并形成ETs。这种细胞死亡形式既非凋亡也非坏死,但它是否像其他ROS介导的信号级联反应那样是由于磷酸酶和激酶的氧化而发生,仍有待阐明。这些发现表明“ETosis”是白细胞中一种新的细胞死亡途径。

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