ReviewFrontiers in immunology2016
NETosis as Source of Autoantigens in Rheumatoid Arthritis.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed, 139 citations in OpenAlex.
- Recent Advances in Fluorescent Probes for Imaging Enzyme Activity in NETosis.Chembiochem : a European journal of chemical biology · 2026Review
- Dysregulation of the DNA repair‑immune axis: Targeted therapeutic strategies for autoimmune diseases (Review).International journal of molecular medicine · 2026Review
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- The Ability of Probiotic Strain Escherichia coli O83:K24:H31 to Modulate Gut Homeostasis and Immune Function After Antibiotic-Induced Dysbiosis.Probiotics and antimicrobial proteins · 2026Article
- Neutrophil extracellular traps in rheumatoid arthritis: biomarkers, drivers, and emerging therapeutic targets.Clinical and experimental immunology · 2026Review
- Research progress on neutrophil extracellular traps and hepatitis-to-hepatocellular carcinoma transformation (Review).Oncology letters · 2026Review
- Neutrophil Extracellular Traps in Wound Healing of Diabetes: Mechanisms, Inducers, and Therapeutic Implications.Mediators of inflammation · 2026Review
- Progress of Programmed Cell Death in Steroid-Induced Osteonecrosis of the Femoral Head.Orthopaedic surgery · 2026Review
- Macrophage-centred crosstalk with infiltrating immune cells in rheumatoid arthritis and its regulation by mesenchymal stem cells.Journal of translational medicine · 2025Review
- Review
- Glycosaminoglycans activate peptidylarginine deiminase 4 by enhancing calcium affinity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- How the Cigarette Fire Burns the Rheumatoid Joints.JMA journal · 2025Article
- Role of Neutrophils in Homeostasis and Diseases.MedComm · 2025Review
- Animal Models in Rheumatoid Arthritis: Is There a Correlation Between Autoantibodies in Human Pathology and Animal Models?Biology · 2025Review
- Synovial Fluid as a Crucial Component of the Joint Microenvironment in Rheumatoid Arthritis.Immune network · 2025Review
- Microbial players in autoimmunity: multicentric analysis of the association betweenMicrobiology spectrum · 2025Article
- Tissue-resident immune cells: from defining characteristics to roles in diseases.Signal transduction and targeted therapy · 2025Review
- NETs promote invasive behavior of fibroblast-like synoviocytes through GPIbα in rheumatoid arthritis.Frontiers in immunology · 2025Article
- IL33-induced neutrophil extracellular traps (NETs) mediate a positive feedback loop for synovial inflammation and NET amplification in rheumatoid arthritis.Experimental & molecular medicine · 2024Article
- Regulation of neutrophil associated RNASET2 expression in rheumatoid arthritis.Scientific reports · 2024Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
In neutrophils (but also in eosinophils and in mast cells), different inflammatory stimuli induce histone deimination, chromatin decondensation, and NET formation. These web-like structures that trap and kill microbes contain DNA, cationic granule proteins, and antimicrobial peptides, but the most abundant proteins are core histones. Histones contained in NETs have been deiminated, and arginines are converted in citrullines. While deimination is a physiological process amplified in inflammatory conditions, only individuals carrying genetic predisposition to develop rheumatoid arthritis (RA) make antibodies to deiminated proteins. These antibodies, collectively identified as anti-citrullinated proteins/peptides antibodies (ACPA), react with different deiminated proteins and display partially overlapping specificities. In this paper, we will summarize current evidence supporting the role of NETosis as critical mechanism in the breach of tolerance to self-antigens and in supporting expansion and differentiation of autoreactive cells. In fact, several lines of evidence connect NETosis with RA: RA unstimulated synovial fluid neutrophils display enhanced NETosis; sera from RA patients with Felty's syndrome bind deiminated H3 and NETs; a high number of RA sera bind deiminated H4 contained in NETs; human monoclonal antibodies generated from RA synovial B cells decorate NETs and bind deiminated histones. In RA, NETs represent on one side an important source of autoantigens bearing posttranslational modifications and fueling the production of ACPA. On the other side, NETs deliver signals that maintain an inflammatory milieu and contribute to the expansion and differentiation of ACPA-producing B cells.
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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.