ArticleImmunology2017
Neither eosinophils nor neutrophils require ATG5-dependent autophagy for extracellular DNA trap formation.
Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
63 citing papers in PubMed, 87 citations in OpenAlex.
- Eosinophil extracellular traps: heterogeneity of their stimuli, components, and functions.Trends in cell biology · 2026Review
- Programmed Cell Death in Chronic Rhinosinusitis.Clinical and translational allergy · 2026Review
- Autophagy, NET formation, and inflammation crosstalk in thrombotic autoimmune diseases.Frontiers in immunology · 2026Review
- Neutrophils in Tissue Injury and Repair: Molecular Mechanisms and Therapeutic Targets.MedComm · 2025Review
- Extracellular Traps in Inflammation: Pathways and Therapeutic Targets.Life (Basel, Switzerland) · 2025Review
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- Neutrophil Extracellular Traps in Sepsis and Sepsis-Related Organ Dysfunction.ImmunoTargets and therapy · 2025Review
- Eosinophil extracellular traps in respiratory ailment: Pathogenic mechanisms and clinical translation.World journal of otorhinolaryngology - head and neck surgery · 2024Review
- The role of extracellular traps released by neutrophils, eosinophils, and macrophages in asthma.Respiratory research · 2024Review
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- Review
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- ATG5 provides host protection acting as a switch in the atg8ylation cascade between autophagy and secretion.Developmental cell · 2023Article
- Neutrophil CEACAM1 determines susceptibility to NETosis by regulating the S1PR2/S1PR3 axis in liver transplantation.The Journal of clinical investigation · 2023Article
- Syntaxin-4 and SNAP23 are involved in neutrophil degranulation, but not in the release of mitochondrial DNA during NET formation.Frontiers in immunology · 2023Article
- The Role of Macrophage Autophagy in Asthma: A Novel Therapeutic Strategy.Mediators of inflammation · 2023Review
- Autophagy and Its Lineage-Specific Roles in the Hematopoietic System.Oxidative medicine and cellular longevity · 2023Review
- The regulatory role of eosinophils in adipose tissue depends on autophagy.Frontiers in immunology · 2023Article
- New insights into autophagy in inflammatory subtypes of asthma.Frontiers in immunology · 2023Review
- Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis.Clinical and translational medicine · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of extracellular traps (ETs) in innate immunity is well established, but the molecular mechanisms responsible for their formation remain unclear and in scientific dispute. ETs have been defined as extracellular DNA scaffolds associated with the granule proteins of eosinophils or neutrophils. They are capable of killing bacteria extracellularly. Based mainly on results with phosphoinositide 3-kinase (PI3K) inhibitors such as 3-methyladenine (3-MA) and wortmannin, which are commonly used to inhibit autophagy, several groups have reported that autophagy is required for neutrophil extracellular trap (NET) formation. We decided to investigate this apparent dependence on autophagy for ET release and generated genetically modified mice that lack, specifically in eosinophils or neutrophils, autophagy-related 5 (Atg5), a gene encoding a protein essential for autophagosome formation. Interestingly, neither eosinophils nor neutrophils from Atg5-deficient mice exhibited abnormalities in ET formation upon physiological activation or exposure to low concentrations of PMA, although we could confirm that human and mouse eosinophils and neutrophils, after pre-treatment with inhibitors of class III PI3K, show a block both in reactive oxygen species (ROS) production and in ET formation. The so-called late autophagy inhibitors bafilomycin A1 and chloroquine, on the other hand, were without effect. These data indicate that ET formation occurs independently of autophagy and that the inhibition of ROS production and ET formation in the presence of 3-MA and wortmannin is probably owing to their additional ability to block the class I PI3Ks, which are involved in signalling cascades initiated by triggers of ET formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.