ArticleBlood2015
Neutrophil oxidative burst activates ATM to regulate cytokine production and apoptosis.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 77 citations in OpenAlex.
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- Caspase-8 silences cell death-independent constitutive immune activation driven by tonic TNF-α.EMBO reports · 2026Article
- Skin-derived G-CSF activates pathological granulopoiesis upon psoriasis.EMBO molecular medicine · 2026Article
- Hematopoietic Aging and Leukemia: Mechanistic and Therapeutic Insights.International journal of molecular sciences · 2026Review
- Altered neutrophil signalling linked to impaired chemotaxis and increased ROS and NET production in older people with frailty.Clinical and experimental immunology · 2026Article
- Characterization of human CD34iScience · 2025Article
- Nutritional status and metabolic alterations in patients with ataxia-telangiectasia.Orphanet journal of rare diseases · 2025Article
- Drug repurposing of cyclin-dependent kinase inhibitors for neutrophilic acute respiratory distress syndrome and psoriasis.Journal of advanced research · 2025Review
- Acute Exposure to Aerosolized Nanoplastics Modulates Redox-Linked Immune Responses in Human Airway Epithelium.Antioxidants (Basel, Switzerland) · 2025Article
- Identification and validation of biomarkers related to ferroptosis in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- New insights into constitutive neutrophil death.Cell death discovery · 2025Review
- Translational insights from EAE models : decoding MOGAD pathogenesis and therapeutic innovation.Frontiers in immunology · 2025Review
- How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation.Biomolecules · 2024Review
- Neutrophils cultured ex vivo from CD34Journal of translational medicine · 2024Article
- Clinical presentation, diagnosis, and treatment of chronic granulomatous disease.Frontiers in pediatrics · 2024Review
- The role of the neutrophil-lymphocyte ratio in predicting poor outcomes in COVID-19 patients.Cardiology journal · 2024Observational
- ncRNAs-mediated overexpression of STIL predict unfavorable prognosis and correlated with the efficacy of immunotherapy of hepatocellular carcinoma.Cancer cell international · 2023Article
- Neutrophil extracellular traps: from physiology to pathology.Cardiovascular research · 2022Review
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Authors and funding
10 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils play an essential role in the initial stages of inflammation by balancing pro- and antiinflammatory signals. Among these signals are the production of proinflammatory cytokines and the timely initiation of antiinflammatory cell death via constitutive apoptosis. Here we identify ataxia-telangiectasia mutated (ATM) kinase as a modulator of these neutrophil functions. Ataxia-telangiectasia (AT) is a pleiotropic multisystem disorder caused by mutations in the gene-encoding ATM, a master regulator of the DNA damage response. In addition to progressive neurodegeneration and high rates of cancer, AT patients have numerous symptoms that can be linked to chronic inflammation. We report that neutrophils isolated from patients with AT overproduce proinflammatory cytokines and have a prolonged lifespan compared with healthy controls. This effect is partly mediated by increases in activation of p38 MAP kinase. Furthermore, we show that the oxidative burst, catalyzed by nicotinamide adenine dinucleotide phosphate oxidase, can activate ATM in neutrophils. Finally, activation of ATM and DNA damage signaling suppress cytokine production and can abrogate the overproduction of IL-8 in ROS-deficient cells. This reveals a novel mechanism for the regulation of cytokine production and apoptosis, establishing DNA damage as a downstream mediator of immune regulation by reactive oxygen species. We propose that deficiencies in the DNA damage response, like deficiencies in the oxidative burst seen in chronic granulomatous disease, could lead to pathologic inflammation.
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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.