ArticleJCI insight2017
Activated signature of antiphospholipid syndrome neutrophils reveals potential therapeutic target.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
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
60 citing papers in PubMed, 105 citations in OpenAlex.
- Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations.Frontiers in immunology · 2019Trial
- Role of CMTM6 in disease pathogenesis and clinical translation potential (Review).Molecular medicine reports · 2026Review
- Deciphering Platelet Transcriptomic Profiles in Antiphospholipid Syndrome: Insights into Their Role as Immunological Players.International journal of molecular sciences · 2026Article
- Molecular Stratification of Antiphospholipid Syndrome Through Integrative Analysis of the Whole-Blood RNA Transcriptome.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- The role of neutrophil extracellular traps in antiphospholipid syndrome.Frontiers in immunology · 2026Review
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- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- "The NET effect": Neutrophil extracellular traps-a potential key component of the dysregulated host immune response in sepsis.Critical care (London, England) · 2025Review
- A proteomic map of thromboinflammatory signatures in antiphospholipid syndrome: results from antiphospholipid syndrome alliance for clinical trials and international networking (APS ACTION) registry.Frontiers in immunology · 2025Article
- Identification of shared biomarkers and potential therapeutic targets for antiphospholipid syndrome and recurrent miscarriage by integrated bioinformatics analysis and machine learning.Frontiers in medicine · 2025Article
- Mechanism of antiphospholipid antibody-mediated thrombosis in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- Disentangling the riddle of systemic lupus erythematosus with antiphospholipid syndrome: blood transcriptome analysis reveals a less-pronounced IFN-signature and distinct molecular profiles in venous versus arterial events.Annals of the rheumatic diseases · 2024Article
- Reflections on Targeting Neutrophil Extracellular Traps in Deep Vein Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Neutrophil glucose flux as a therapeutic target in antiphospholipid syndrome.The Journal of clinical investigation · 2024Article
- Rethinking antiphospholipid syndrome to guide future management and research.Nature reviews. Rheumatology · 2024Review
- New advances in genomics and epigenetics in antiphospholipid syndrome.Rheumatology (Oxford, England) · 2024Review
- Transmembrane Protein CMTM6 Alleviates Ocular Inflammatory Response and Improves Corneal Epithelial Barrier Function in Experimental Dry Eye.Investigative ophthalmology & visual science · 2024Article
- The role of P-selectin/PSGL-1 in regulating NETs as a novel mechanism in cerebral ischemic injury.Frontiers in neurology · 2024Review
- Surface Geometry of Cargo-less Gold Nanoparticles Is a Driving Force for Selective Targeting of Activated Neutrophils to Reduce Thrombosis in Antiphospholipid Syndrome.Nano letters · 2023Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Antiphospholipid antibodies, present in one-third of lupus patients, increase the risk of thrombosis. We recently reported a key role for neutrophils - neutrophil extracellular traps (NETs), in particular - in the thrombotic events that define antiphospholipid syndrome (APS). To further elucidate the role of neutrophils in APS, we performed a comprehensive transcriptome analysis of neutrophils isolated from patients with primary APS. Moreover, APS-associated venous thrombosis was modeled by treating mice with IgG prepared from APS patients, followed by partial restriction of blood flow through the inferior vena cava. In patients, APS neutrophils demonstrated a proinflammatory signature with overexpression of genes relevant to IFN signaling, cellular defense, and intercellular adhesion. For in vivo studies, we focused on P-selectin glycoprotein ligand-1 (PSGL-1), a key adhesion molecule overexpressed in APS neutrophils. The introduction of APS IgG (as compared with control IgG) markedly potentiated thrombosis in WT mice, but not PSGL-1-KOs. PSGL-1 deficiency was also associated with reduced leukocyte vessel wall adhesion and NET formation. The thrombosis phenotype was restored in PSGL-1-deficient mice by infusion of WT neutrophils, while an anti-PSGL-1 monoclonal antibody inhibited APS IgG-mediated thrombosis in WT mice. PSGL-1 represents a potential therapeutic target in APS.
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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.