ArticleAnnals of the rheumatic diseases2017
Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome.
Article in Annals of the rheumatic diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.
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Who cites it
36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Pooled it
- Pooled it
- Non-medical Switching from Originator Tumor Necrosis Factor Inhibitors to Their Biosimilars: Systematic Review of Randomized Controlled Trials and Real-World Studies.Advances in therapy · 2018Pooled it
- Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations.Frontiers in immunology · 2019Trial
- Metabolic Complications in Autoimmune and Autoinflammatory Diseases: Pathophysiology, Clinical Implications, and Therapeutic Perspectives.Journal of clinical medicine · 2026Review
- RNA sequencing-derived gene co-expression and drug-gene interaction analysis reveal STAT1 as a potential therapeutic target in thrombotic antiphospholipid syndrome.Frontiers in immunology · 2026Article
- Perspective on Renal Involvement in Antiphospholipid Syndrome: Implications for Diagnosis, Pathogenesis, and Treatment.Journal of clinical medicine · 2025Review
- Antiphospholipid Antibodies as Key Players in Systemic Lupus Erythematosus: The Relationship with Cytokines and Immune Dysregulation.International journal of molecular sciences · 2024Review
- Proteomics of Serum Samples for the Exploration of the Pathological Mechanism of Obstetric Antiphospholipid Syndrome.Journal of proteome research · 2024Article
- Type I interferon pathway activation across the antiphospholipid syndrome spectrum: associations with disease subsets and systemic antiphospholipid syndrome presentation.Frontiers in immunology · 2024Article
- Endothelial Progenitor Cells in Autoimmune Disorders.Stem cell reviews and reports · 2023Review
- The Role of Neutrophil Extracellular Traps (NETs) in the Pathogenesis of Systemic Lupus Erythematosus and Antiphospholipid Syndrome.International journal of molecular sciences · 2023Article
- The ABCs of antiphospholipid syndrome.Archives of rheumatology · 2023Review
- Defibrotide Inhibits Antiphospholipid Antibody-Mediated Neutrophil Extracellular Trap Formation and Venous Thrombosis.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- An Update on Antiphospholipid Syndrome.Current rheumatology reports · 2022Review
- Dendritic Cells and Antiphospholipid Syndrome: An Updated Systematic Review.Life (Basel, Switzerland) · 2021Review
- Utilizing type I interferon expression in the identification of antiphospholipid syndrome subsets.Expert review of clinical immunology · 2021Review
- Linking clotting and autoimmunity.Science (New York, N.Y.) · 2021Article
- Potential Implications of a Type 1 Interferon Gene Signature on COVID-19 Severity and Chronic Inflammation in Sickle Cell Disease.Frontiers in medicine · 2021Article
- Review
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
objectivesPatients with antiphospholipid syndrome (APS) are at risk for subclinical endothelial injury, as well as accelerated atherosclerosis. In the related disease systemic lupus erythematosus, there is a well-established defect in circulating endothelial progenitors, which leads to an accrual of endothelial damage over time. This defect has been at least partially attributed to exaggerated expression of type I interferons (IFNs). We sought to determine whether these pathways are important in APS.
methodsWe studied 68 patients with primary APS. Endothelial progenitors were assessed by flow cytometry and functional assay. Type I IFN activity was determined by a well-accepted bioassay, while peripheral blood mononuclear cells were scored for expression of IFN-responsive genes.
resultsEndothelial progenitors from patients with APS demonstrated a marked defect in the ability to differentiate into endothelial cells, a phenotype which could be mimicked by treating control progenitors with APS sera. Elevated type I IFN activity was detected in the circulation of patients with APS (a finding that was then replicated in an independent cohort). While IgG depletion from APS sera did not rescue endothelial progenitor function, the dysfunction was successfully reversed by a type I IFN receptor-neutralising antibody.
conclusionsWe describe, for the first time to our knowledge, an IFN signature in primary APS and show that this promotes impaired endothelial progenitor function. This work opens the door to novel approaches that may mitigate vascular damage in APS, such as anti-IFN drugs.
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