ArticleScience translational medicine2011
Neutrophils activate plasmacytoid dendritic cells by releasing self-DNA-peptide complexes in systemic lupus erythematosus.
Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 715 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
715 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,255 citations in OpenAlex.
- Characteristics and Role of Neutrophil Extracellular Traps in Asthma.Inflammation · 2022Pooled it
- Safety and clinical activity of autologous RNA chimeric antigen receptor T-cell therapy in myasthenia gravis (MG-001): a prospective, multicentre, open-label, non-randomised phase 1b/2a study.The Lancet. Neurology · 2023Trial
- Antimicrobial proteins regulating neuroinflammation.Annals of medicine · 2026Review
- Circulating cell-free DNA as a biomarker in systemic lupus erythematosus: A narrative review.Journal of translational autoimmunity · 2026Review
- Disease modification in lupus nephritis: towards a pathophysiology-based treatment paradigm.Nature reviews. Nephrology · 2026Review
- Review
- Basophil Extracellular Traps in Immunity and Disease.Cancers · 2026Review
- IFNAR1-dependent metabolic circuit drives pathogenic neutrophil activation in chronic mucosal inflammation.Signal transduction and targeted therapy · 2026Article
- TLR7/9 and type I interferon signaling reprogram neutrophil NET responses and impair antibacterial defense in systemic lupus erythematosus.Cell press blue · 2026Article
- Building Blocks of 2,3-Diaminopropionic Acid Functionalized with an Oxa-Acid Spacer Shift the Functional Profile of Human Cathelicidin LL-37: Enhanced Enzymatic Stability and Selective Suppression of Neutrophil Degranulation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- dsDNA-Induced AIM2 Pyroptosis in Glomerular Endothelial Cells Aggravate Lupus Nephritis.Cell biochemistry and biophysics · 2026Article
- LL-37 IgG levels are associated with clinical characteristics and T follicular cell response in acute coronary syndrome in adults.Physiological reports · 2026Article
- Review
- Elevated neutrophil extracellular traps predict mortality and CKD progression in critically ill AKI patients: a prospective observational study.International urology and nephrology · 2026Observational
- Multi-faceted characterization of the gut microbiome and metabolome in patients with primary Sjögren syndrome.Cell reports. Medicine · 2026Article
- Human cathelicidin peptide LL-37 compacts nucleic acids and alters neutrophil extracellular trap structure.Scientific reports · 2026Article
- From pathogenesis to precision medicine in systemic lupus erythematosus: Emerging biomarkers and targeted interventions.iScience · 2026Review
- Age- and tissue-dependent diversity of human plasmacytoid dendritic cells uncovers a cycling subset dominant in early life and cancer.Immunity · 2026Article
655 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a severe and incurable autoimmune disease characterized by chronic activation of plasmacytoid dendritic cells (pDCs) and production of autoantibodies against nuclear self-antigens by hyperreactive B cells. Neutrophils are also implicated in disease pathogenesis; however, the mechanisms involved are unknown. Here, we identified in the sera of SLE patients immunogenic complexes composed of neutrophil-derived antimicrobial peptides and self-DNA. These complexes were produced by activated neutrophils in the form of web-like structures known as neutrophil extracellular traps (NETs) and efficiently triggered innate pDC activation via Toll-like receptor 9 (TLR9). SLE patients were found to develop autoantibodies to both the self-DNA and antimicrobial peptides in NETs, indicating that these complexes could also serve as autoantigens to trigger B cell activation. Circulating neutrophils from SLE patients released more NETs than those from healthy donors; this was further stimulated by the antimicrobial autoantibodies, suggesting a mechanism for the chronic release of immunogenic complexes in SLE. Our data establish a link between neutrophils, pDC activation, and autoimmunity in SLE, providing new potential targets for the treatment of this devastating disease.
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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.