Viable neutrophils release mitochondrial DNA to form neutrophil extracellular traps

By S. Yousefi, Cristina C. Mihalache, E. Kozlowski, Inès Schmid, H. Simon. Cell Death and Differentiation, 2009

997 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/33c9bfc8506213ab11cd4150fe4a50c76a387525

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In Immunology

Citations in the corpus

NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis (2013, result): “In contrast, as previously reported (21), control and RA neutrophils exposed to GM-CSF without other priming stimuli did not display increased NET formation (Fig.”
Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality (2011, positive): “context broader than cell death because they observed that even viable eosinophils and neutrophils release extracellular traps.(19,63) In these studies, eosinophils and neutrophils were pretreated with the pro-inflammatory cytokines IL-5þ IFNg or with GM-CSFþC5a, respectively.”
Neutrophil extracellular traps (NETs): Double-edged swords of innate immunity (2012, background): “protease extrusion mechanism from intact neutrophils, where mitochondrial DNA release is apparently not associated to cell death (16).”
NETosis: how vital is it? (2013, background): “Additionally, Yousefi and colleagues, first in eosinophils but subsequently in neutrophils, described a form of NETosis that caused a catapult of the DNA from mitochondria without causing lytic cellular death.(42,43) Conversely, a new report describes eosinophil trap formation resulting in cytolytic”
Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “Nevertheless, mitochondrial DNA is released following physiological stimuli and may represent a distinct form of NET formation [58].”
A Novel Mechanism of Rapid Nuclear Neutrophil Extracellular Trap Formation in Response to Staphylococcus aureus (2010, background): “Recent studies suggested that mitochondrial DNA could be released from both eosinophils (11) and neutrophils (12).”
Mitochondrial DNA in inflammation and immunity (2020, positive): “Within minutes of stimulation, neutrophils rapidly produce NETs, whereas the death of neutrophils (dubbed “NETosis”) occurs ~ 2 h after [160].”
Neutrophil Extracellular Traps and Its Implications in Inflammation: An Overview (2017, background): “Finally, Yousefi has described another type of vital NETosis dependent on ROS, in which mitochondrial DNA is released instead of nuclear DNA; this process results in NET formation from 80% of neutrophils within 15 min through recognition of C5a or lipopolysaccharide (LPS) (29).”
Neutrophils, from marrow to microbes. (2010, background): “…that extracellular strands of DNA may also be generated from mitochondria from activated neutrophils in a process that was compatible with full neutrophil activity after NET formation, thus indicating an alternative to NET formation as a death mechanism of neutrophils (Yousefi et al., 2009).”
Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012 (2011, background): “demonstrated by several observations: (i) no cytosolic proteins are detected in NETs; (ii) NET-releasing cells fail to take up exclusion dyes; and (iii) NETs can be detected within 30–60 min after stimulation with IL-8 and lipopolysaccharide.(158,159) However, following non-physiological stimulation”
The neutrophil in vascular inflammation (2011, background): “In separate studies, eosinophils and neutrophils were found to catapult their DNA out of the cell into the extracellular space, but the DNA source was non-nuclear and, instead, the DNA originated from the mitochondria 82, 83 .”
Extracellular DNA traps promote thrombosis (2010, background): “Positive stainingusing anantibody specific forDNA/ histone complex showed that the DNA was of nuclear rather than mitochondrial origin (26) (Fig.”