ETosis : A Novel Cell Death Pathway
ETosis : A Novel Cell Death Pathway
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DOI：
10.1126/stke.121pe25
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发表时间：
2008-05-27
影响因子：
7.3
通讯作者：
Henriques-Normark, Birgitta
中科院分区：
文献类型：
--
作者：
Wartha, Florian;Henriques-Normark, Birgitta
嗜中性粒细胞和肥大细胞形成细胞外陷阱（Extracellular trap，EAT）是先天性免疫应答的重要机制。这些结构由染色质-DNA骨架和附着的抗菌肽和酶组成，这些抗菌肽和酶可以捕获和杀死微生物。用佛波醇酯、化学引诱肽或趋化因子刺激嗜中性粒细胞和肥大细胞后，通过NAPDH烟酰胺腺嘌呤二核苷酸磷酸（还原型）]氧化酶产生活性氧（ROS），如过氧化氢，启动信号级联反应，导致核膜和细胞膜崩解并形成脂质体。这种形式的细胞死亡既不是凋亡性的也不是坏死性的，但它是否是因为磷酸酶和激酶的氧化而发生的，就像在其他ROS介导的信号级联中一样，仍有待阐明。这些发现暗示“ETosis”是白细胞中的一种新的细胞死亡途径。
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 (reducedform)] 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.