The Expanding Role of Extracellular Traps in Inflammation and Autoimmunity: The New Players in Casting Dark Webs
Open accessPreprint — published as 10.3390/ijms23073793
Abstract
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.
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Two forms of NETosis have been described: classical or suicidal NETosis, leading to cell death, and vital NETosis, where the cell retains its viability and many effector functions.
“Two forms of NETosis have now been described: classical or suicidal NETosis (leading to cell death), and vital NETosis, where the cell retains its viability and many of its effector functions [62].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [62]
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References 271 · Cited by 65
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- Authors
- Huang, S. U.-S., & O’Sullivan, K. M.
- Affiliations
- Monash University (AU)
- Corresponding author
- O’Sullivan, Kim Maree
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2022-03-01
- Volume
- 23
- Issue
- 7
- Pages
- 3793-3793
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC8998317
- OpenAlex
- W4226072706
- Cited by
- 65
- References
- 271
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 19 · 2023: 14 · 2022: 8
- FWCI
- 1.47
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Preprints.org (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Health and Medical Research Council (2001325)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Epidemiology › Autoimmune and Inflammatory Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Keywords
- neutrophil extracellular traps, NETosis, extracellular traps, inflammation, autoimmunity, neutrophils, macrophages, mast cells, basophils, dendritic cells, eosinophils, extracellular DNA, autoantigens, vasculitis, autoimmune kidney disease, atherosclerosis, rheumatoid arthritis, psoriasis, lung disease, cancer, therapeutic target
- MeSH terms
- Autoimmune Diseases, DNA, Humans, Inflammation, Neutrophils, Autoimmunity, Endothelial Cells, Extracellular Traps
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