Neutrophil Extracellular Traps: The Biology of Chromatin Externalization

被引：271

作者：

Sollberger, Gabriel ^{[1
]}

Tilley, Dorothea Ogmore ^{[1
]}

Zychlinsky, Arturo ^{[1
]}

机构：

[1] Max Planck Inst Infect Biol, Dept Cellular Microbiol, Charitepl 1,Campus Charite Mitte, D-10117 Berlin, Germany

来源：

DEVELOPMENTAL CELL | 2018年 / 44卷 / 05期

基金：

瑞士国家科学基金会;

关键词：

COLONY-STIMULATING FACTOR; PEPTIDYLARGININE DEIMINASE INHIBITION; NET FORMATION; RHEUMATOID-ARTHRITIS; HEMATOPOIETIC STEM; ENDOTHELIAL DAMAGE; DISEASE SEVERITY; FACTOR-RECEPTOR; MICE LACKING; DNA TRAPS;

D O I：

10.1016/j.devcel.2018.01.019

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Neutrophils are essential to the homeostatic mission of safeguarding host tissues, responding rapidly and diversely to breaches of the host's barriers to infection, and returning tissues to a sterile state. In response to specific stimuli, neutrophils extrude modified chromatin structures decorated with specific cytoplasmic and granular proteins called neutrophil extracellular traps (NETs). Several pathways lead to this unique form of cell death (NETosis). Extracellular chromatin may have evolved to defend eukaryotic organisms against infection, and its release has at least three functions: trapping and killing of microbes, amplifying immune responses, and inducing coagulation. Here we review neutrophil development and heterogeneity with a focus on NETs, NET formation, and their relevance in host defense and disease.

引用

页码：542 / 553

页数：12

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