ArticlePloS one2015
Platelet Activation and Thrombus Formation over IgG Immune Complexes Requires Integrin αIIbβ3 and Lyn Kinase.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 32 citations in OpenAlex.
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Immobilized IgG-containing immune complexes require platelets to recruit neutrophils during inflammation.The Journal of clinical investigation · 2026Article
- Platelets in systemic lupus erythematosus: from hemostatic allies to pathogenic drivers.Frontiers in immunology · 2026Review
- Persistent Chronic Thrombo-Inflammation in Anti-Glomerular Basement Membrane Disease Despite Immune Complex Removal.Kidney international reports · 2025Article
- The Relationship of Platelets With the Clinical Manifestations and Serologic Markers in Systemic Lupus Erythematosus: A Single-Center Retrospective Study.Immunity, inflammation and disease · 2025Article
- Coagulopathy during COVID-19 infection: a brief review.Clinical and experimental medicine · 2023Review
- Article
- The Contribution of Neutrophils and NETs to the Development of Type 1 Diabetes.Frontiers in immunology · 2022Review
- Prothrombotic Phenotype in COVID-19: Focus on Platelets.International journal of molecular sciences · 2021Review
- FcγRIIA expression accelerates nephritis and increases platelet activation in systemic lupus erythematosus.Blood · 2020Article
- Biphasic Force-Regulated Phosphorylation Site Exposure and Unligation of ERM Bound with PSGL-1: A Novel Insight into PSGL-1 Signaling via Steered Molecular Dynamics Simulations.International journal of molecular sciences · 2020Article
- Platelets Disseminate Extracellular Vesicles in Lymph in Rheumatoid Arthritis.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- In systemic lupus erythematosus anti-dsDNA antibodies can promote thrombosis through direct platelet activation.Journal of autoimmunity · 2020Article
- Platelets: emerging facilitators of cellular crosstalk in rheumatoid arthritis.Nature reviews. Rheumatology · 2019Review
- The genomic organization and expression pattern of the low-affinity Fc gamma receptors (FcγR) in the Göttingen minipig.Immunogenetics · 2019Article
- Adhesion structures in leukemia cells and their regulation by Src family kinases.Cell adhesion & migration · 2018Article
- The non-haemostatic role of platelets in systemic lupus erythematosus.Nature reviews. Rheumatology · 2018Review
- New Insights on Platelets and Platelet-Derived Microparticles in Systemic Lupus Erythematosus.Current rheumatology reports · 2017Review
- The expression of fibronectin is significantly suppressed in macrophages to exert a protective effect against Staphylococcus aureus infection.BMC microbiology · 2017Article
- Clustering of glycoprotein VI (GPVI) dimers upon adhesion to collagen as a mechanism to regulate GPVI signaling in platelets.Journal of thrombosis and haemostasis : JTH · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
IgG immune complexes contribute to the etiology and pathogenesis of numerous autoimmune disorders, including heparin-induced thrombocytopenia, systemic lupus erythematosus, rheumatoid- and collagen-induced arthritis, and chronic glomerulonephritis. Patients suffering from immune complex-related disorders are known to be susceptible to platelet-mediated thrombotic events. Though the role of the Fc receptor, FcγRIIa, in initiating platelet activation is well understood, the role of the major platelet adhesion receptor, integrin αIIbβ3, in amplifying platelet activation and mediating adhesion and aggregation downstream of encountering IgG immune complexes is poorly understood. The goal of this investigation was to gain a better understanding of the relative roles of these two receptor systems in immune complex-mediated thrombotic complications. Human platelets, and mouse platelets genetically engineered to differentially express FcγRIIa and αIIbβ3, were allowed to interact with IgG-coated surfaces under both static and flow conditions, and their ability to spread and form thrombi evaluated in the presence and absence of clinically-used fibrinogen receptor antagonists. Although binding of IgG immune complexes to FcγRIIa was sufficient for platelet adhesion and initial signal transduction events, platelet spreading and thrombus formation over IgG-coated surfaces showed an absolute requirement for αIIbβ3 and its ligands. Tyrosine kinases Lyn and Syk were found to play key roles in IgG-induced platelet activation events. Taken together, our data suggest a complex functional interplay between FcγRIIa, Lyn, and αIIbβ3 in immune complex-induced platelet activation. Future studies may be warranted to determine whether patients suffering from immune complex disorders might benefit from treatment with anti-αIIbβ3-directed therapeutics.
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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.