ArticleArthritis & rheumatology (Hoboken, N.J.)2021
Association of the Leukocyte Immunoglobulin-like Receptor A3 Gene With Neutrophil Activation and Disease Susceptibility in Adult-Onset Still's Disease.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Autoantibody-Based Models for the Diagnosis and Activity Assessment of Takayasu Arteritis.Journal of cardiovascular translational research · 2026Article
- Still's Disease and Autoinflammation: Positioning an Inflammatory Syndrome on the Autoinflammation-Autoimmunity Spectrum.Current rheumatology reports · 2026Review
- Leukocyte immunoglobulin-like receptor B2 regulates atherosclerosis progression by modulating macrophage extracellular trap formation in foam macrophages through the PI3K-AKT signaling pathway.Journal of cell communication and signaling · 2025Article
- Genome-Wide Association Analysis Identifies LILRB2 Gene for Pathological Myopia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- Recent advances and evolving concepts in Still's disease.Nature reviews. Rheumatology · 2024Review
- Cytokine Storm Syndrome Associated with Systemic Juvenile Idiopathic Arthritis.Advances in experimental medicine and biology · 2024Review
- AIM2 and NLRC4-driven inflammasome activation in adult-onset Still's disease and the preliminary therapeutic effect exploration of carboxyamidotriazole.Clinical rheumatology · 2023Article
- Dermatologic Manifestations of Noninflammasome-Mediated Autoinflammatory Diseases.JID innovations : skin science from molecules to population health · 2023Review
- Human leukocyte immunoglobulin-like receptors in health and disease.Frontiers in immunology · 2023Review
- Soluble LILRA3 is aberrantly expressed in antiphospholipid syndrome (APS) and is a potential marker of thrombotic APS.Rheumatology (Oxford, England) · 2022Article
- Adult-onset Still's disease: A disease at the crossroad of innate immunity and autoimmunity.Frontiers in medicine · 2022Review
- Activation mechanisms of monocytes/macrophages in adult-onset Still disease.Frontiers in immunology · 2022Review
- An Update on the Pathogenic Role of Neutrophils in Systemic Juvenile Idiopathic Arthritis and Adult-Onset Still's Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAdult-onset Still's disease (AOSD) is a severe autoinflammatory disease. Neutrophil activation with enhanced neutrophil extracellular trap (NET) formation is involved in the pathogenesis of AOSD. Functional leukocyte immunoglobulin-like receptor A3 (LIR-A3; gene name LILRA3) has been reported to be associated with many autoimmune diseases. We aimed to investigate the association of LILRA3 with disease susceptibility and neutrophil activation in AOSD.
methodsThe LILRA3 deletion polymorphism and its tagging single-nucleotide polymorphism rs103294 were genotyped in 164 patients with AOSD and 305 healthy controls. The impact of LILRA3 on clinical features and messenger RNA expression was evaluated. Plasma levels of LIR-A3 were detected using enzyme-linked immunosorbent assay (ELISA), and the correlation between LIR-A3 plasma levels and disease activity and levels of circulating NET-DNA was investigated. LIR-A3-induced NETs were determined using PicoGreen double-stranded DNA dye and immunofluorescence analysis in human neutrophils and a neutrophil-like differentiated NB4 cell line transfected with LIR-B2 small interfering RNA.
resultsThe findings from genotyping demonstrated that functional LILRA3 was a risk factor for AOSD (11% in AOSD patients versus 5.6% in healthy controls; odds ratio 2.089 [95% confidence interval 1.030-4.291], P = 0.034), and associated with leukocytosis (P = 0.039) and increased levels of circulating neutrophils (P = 0.027). Functional LILRA3 messenger RNA expression was higher in the peripheral blood mononuclear cells (P < 0.0001) and neutrophils (P < 0.001) of LILRA3
conclusionOur study provides the first evidence that functional LILRA3 is a novel genetic risk factor for the development of AOSD and that functional LIR-A3 may play a pathogenic role by inducing formation of NETs.
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