Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality
Open Access
- 4 February 2011
- journal article
- review article
- Published by Springer Science and Business Media LLC in Cell Death & Differentiation
- Vol. 18 (4), 581-588
- https://doi.org/10.1038/cdd.2011.1
Abstract
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.Keywords
This publication has 97 references indexed in Scilit:
- Neutrophil extracellular trap cell death requires both autophagy and superoxide generationCell Research, 2010
- In Vivo Requirement for Atg5 in Antigen Presentation by Dendritic CellsImmunity, 2010
- NETs: a new strategy for using old weaponsTrends in Immunology, 2009
- Extracellular histones are major mediators of death in sepsisNature Medicine, 2009
- Netting neutrophils in autoimmune small-vessel vasculitisNature Medicine, 2009
- Toll-like receptors control autophagyThe EMBO Journal, 2008
- Autophagy in the Pathogenesis of DiseaseCell, 2008
- Toll-like Receptor 4 Is a Sensor for Autophagy Associated with Innate ImmunityImmunity, 2007
- Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4The EMBO Journal, 2007
- The role of autophagy during the early neonatal starvation periodNature, 2004