Multiple Origins of Extracellular DNA Traps

Ramos-Martínez, E; Hernández-González, Leticia; Ramos-Martínez, Iván; Mayoral, Laura; López-Cortés, Georgina I.; Pérez-Campos, Eduardo; Andrade, Gabriel Mayoral; Hernández-Huerta, María Teresa; José, Marco V.

doi:10.3389/fimmu.2021.621311

Cited by 27 publications

(24 citation statements)

References 154 publications

(157 reference statements)

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“…The common purpose of ETosis in these species is overwhelmingly in defense against pathogenic infection, perhaps a strategy that emerged early on in eukaryotic evolution. Using a congruency test, Ramos-Martinez et al found that the ETs across these species exhibited convergent evolution, and the transition from being unicellular to multicellular organisms was crucial for their emergence [ 42 ].…”

Section: A Brief History Of the Discovery Of Netsmentioning

confidence: 99%

The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs

Huang

O’Sullivan

2022

IJMS

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The first description of a new form of neutrophil cell death distinct from that of apoptosis or necrosis was discovered in 2004 and coined neutrophil extracellular traps “(NETs)” or “NETosis”. Different stimuli for NET formation, and pathways that drive neutrophils to commit to NETosis have been elucidated in the years that followed. Critical enzymes required for NET formation have been discovered and targeted therapeutically. NET formation is no longer restricted to neutrophils but has been discovered in other innate cells: macrophages/monocytes, mast Cells, basophils, dendritic cells, and eosinophils. Furthermore, extracellular DNA can also be extruded from both B and T cells. It has become clear that although this mechanism is thought to enhance host defense by ensnaring bacteria within large webs of DNA to increase bactericidal killing capacity, it is also injurious to innocent bystander tissue. Proteases and enzymes released from extracellular traps (ETs), injure epithelial and endothelial cells perpetuating inflammation. In the context of autoimmunity, ETs release over 70 well-known autoantigens. ETs are associated with pathology in multiple diseases: lung diseases, vasculitis, autoimmune kidney diseases, atherosclerosis, rheumatoid arthritis, cancer, and psoriasis. Defining these pathways that drive ET release will provide insight into mechanisms of pathological insult and provide potential therapeutic targets.

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Section: A Brief History Of the Discovery Of Netsmentioning

confidence: 99%

The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs

Huang

O’Sullivan

2022

IJMS

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“…The eosinophil extracellular traps process also depends on the production of ROS, such as neutrophil and mast cells extracellular traps. mtDNA release was also observed in B, T, and NK cells in response to oligodeoxynucleotides [ 105 ].…”

Section: Mechanisms Of Release Of Mtdna In Biological Fluidsmentioning

confidence: 99%

Molecular Mechanisms of mtDNA-Mediated Inflammation

Gaetano

Solodka

Zanini

et al. 2021

Cells

106

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Besides their role in cell metabolism, mitochondria display many other functions. Mitochondrial DNA (mtDNA), the own genome of the organelle, plays an important role in modulating the inflammatory immune response. When released from the mitochondrion to the cytosol, mtDNA is recognized by cGAS, a cGAMP which activates a pathway leading to enhanced expression of type I interferons, and by NLRP3 inflammasome, which promotes the activation of pro-inflammatory cytokines Interleukin-1beta and Interleukin-18. Furthermore, mtDNA can be bound by Toll-like receptor 9 in the endosome and activate a pathway that ultimately leads to the expression of pro-inflammatory cytokines. mtDNA is released in the extracellular space in different forms (free DNA, protein-bound DNA fragments) either as free circulating molecules or encapsulated in extracellular vesicles. In this review, we discussed the latest findings concerning the molecular mechanisms that regulate the release of mtDNA from mitochondria, and the mechanisms that connect mtDNA misplacement to the activation of inflammation in different pathophysiological conditions.

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“…The common purpose of ETosis in these species is overwhelmingly in defence against pathogenic infection, perhaps a strategy that emerged early on in eukaryotic evolution. Using a congruency test, Ramos-Martinez et al found that the ETs across these species exhibited convergent evolution, and the transition from being unicellular to multicellular organisms was crucial for their emergence (42).…”

Section: A Brief History Of the Discovery Of Netsmentioning

confidence: 99%

The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs

Huang¹,

O’Sullivan²

2022

Preprint

View full text Add to dashboard Cite

The first description of a new form of neutrophil cell death distinct from that of apoptosis or necrosis was discovered in 2004 and coined neutrophil extracellular traps “(NETs)” or “NETosis”. Different stimuli for NET formation, and pathways that drive neutrophils to commit to NETosis have been elucidated in the years that followed. Critical enzymes required for NET formation have been discovered, and targeted therapeutically. NET formation is no longer restricted to neutrophils but has been discovered in other innate cells: Macrophages/Monocytes, Mast Cells, Eosinophils, Basophils, Dendritic cells, and extracellular DNA is extruded from both B and T cells. It has become clear that although this mechanism is thought to enhance host defence by ensnaring bacteria within large webs of DNA to increase bactericidal killing capacity, it is also injurious to innocent bystander tissue. Proteases and enzymes released from extracellular traps (ETs), injure epithelial and endothelial cells perpetuating inflammation. In the context of autoimmunity ETs release over 70 well known autoantigens. ETs are associated with pathology in multiple diseases: lung diseases, vasculitis, autoimmune kidney diseases, atherosclerosis, rheumatoid arthritis and psoriasis. Defining these pathways that drive ET release will provide insight into mechanisms of pathological insult, and provide potential therapeutic targets.

show abstract

Multiple Origins of Extracellular DNA Traps

Cited by 27 publications

References 154 publications

The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs

The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs

Molecular Mechanisms of mtDNA-Mediated Inflammation

The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs

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