Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality

被引：417
作者：
Remijsen, Q. [1 ,2 ]
Kuijpers, T. W. [3 ,4 ]
Wirawan, E. [1 ,2 ]
Lippens, S. [1 ,2 ]
Vandenabeele, P. [1 ,2 ]
Vanden Berghe, T. [1 ,2 ]
机构：
[1] Univ Ghent, Dept Biomed Mol Biol, Mol Signaling & Cell Death Unit, B-9000 Ghent, Belgium
[2] VIB, Dept Mol Biomed Res, Mol Signaling & Cell Death Unit, Ghent, Belgium
[3] Sanquin Res & Landsteiner Lab, Dept Blood Cell Res, Amsterdam, Netherlands
[4] Univ Amsterdam, Acad Med Ctr, Dept Paediat Immunol, Emma Childrens Hosp, NL-1105 AZ Amsterdam, Netherlands
来源：
CELL DEATH AND DIFFERENTIATION | 2011年 / 18卷 / 04期
关键词：
NETosis; autophagy; superoxide; NADPH oxidase; cell death; NEUTROPHIL EXTRACELLULAR TRAPS; AUTOPHAGY GENE ATG5; NADPH OXIDASE; PEPTIDYLARGININE DEIMINASE-4; MITOCHONDRIAL-DNA; STREPTOCOCCUS-PNEUMONIAE; HISTONE DEIMINATION; NET FORMATION; ACTIVATION; APOPTOSIS;
D O I：
10.1038/cdd.2011.1
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Neutrophil extracellular traps (NETs) are chromatin structures loaded with antimicrobial molecules. They can trap and kill various bacterial, fungal and protozoal pathogens, and their release is one of the first lines of defense against pathogens. In vivo, NETs are released during a form of pathogen-induced cell death, which was recently named NETosis. Ex vivo, both dead and viable neutrophils can be stimulated to release NETs composed of either nuclear or mitochondrial chromatin, respectively. In certain pathological conditions, NETs are associated with severe tissue damage or certain auto-immune diseases. This review describes the recent progress made in the identification of the mechanisms involved in NETosis and discusses its interplay with autophagy and apoptosis. Cell Death and Differentiation (2011) 18, 581-588; doi:10.1038/cdd.2011.1; published online 4 February 2011
引用
收藏
页码：581 / 588
页数：8
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