ArticleBlood2020
FcγRIIA expression accelerates nephritis and increases platelet activation in systemic lupus erythematosus.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Association ofFrontiers in immunology · 2025Pooled it
- Thrombomodulin Shapes Thrombo-Inflammatory Interactions in Lupus Nephritis.Scandinavian journal of immunology · 2026Article
- Immune-mediated platelet refractoriness: Mechanisms, diagnostics, and therapeutic breakthroughs.Transfusion medicine (Oxford, England) · 2026Review
- Megakaryocytes Internalize and Are Activated by Immune Complexes.Circulation research · 2026Article
- Platelet FcγRIIA is dispensable for hemostasis and arterial thrombosis in the absence of FcγRIIA-specific extracellular stimuli.Research and practice in thrombosis and haemostasis · 2026Article
- Clotting the Gap Between Mitochondria-Mediated Immunity and Mitochondrial Transfer.Circulation research · 2026Review
- Platelets Outperform Leukocytes in Transcriptomic Liquid Biopsy Profiling of Myeloproliferative Neoplasms.bioRxiv : the preprint server for biology · 2026Article
- Immobilized IgG-containing immune complexes require platelets to recruit neutrophils during inflammation.The Journal of clinical investigation · 2026Article
- Molecular mechanisms of acute inflammation: systemic responses and kidney-specific pathophysiology.Function (Oxford, England) · 2026Review
- Platelets in systemic lupus erythematosus: from hemostatic allies to pathogenic drivers.Frontiers in immunology · 2026Review
- Primary Sjögren's syndrome-associated immune thrombocytopenia: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- Mendelian Randomization and Machine Learning Reveal Immune Cell and Gene Drivers in Systemic Lupus Erythematosus.Brain and behavior · 2025Article
- Persistent Chronic Thrombo-Inflammation in Anti-Glomerular Basement Membrane Disease Despite Immune Complex Removal.Kidney international reports · 2025Article
- Platelets as drivers of immunothrombosis in rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Investigating Overlapping Genetic Factors and Novel Causal Genes in Autoimmune Diseases: A Transcriptome-Wide Association and Multiomics Study.International journal of genomics · 2025Article
- Conjoint analysis of methylation, transcriptomic, and proteomic profiles in pemphigus vulgaris.Orphanet journal of rare diseases · 2024Article
- Mechanism of Bile Acid in Regulating Platelet Function and Thrombotic Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A Novel Pathway of Platelet Activation in ACS Mediated by LL-37 Immunoglobulin G Autoantibody Immune Complexes.JACC. Basic to translational science · 2024Article
- SARS-CoV-2 infection modifies the transcriptome of the megakaryocytes in the bone marrow.Blood advances · 2024Article
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 2 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by deposits of immune complexes (ICs) in organs and tissues. The expression of FcγRIIA by human platelets, which is their unique receptor for immunoglobulin G antibodies, positions them to ideally respond to circulating ICs. Whereas chronic platelet activation and thrombosis are well-recognized features of human SLE, the exact mechanisms underlying platelet activation in SLE remain unknown. Here, we evaluated the involvement of FcγRIIA in the course of SLE and platelet activation. In patients with SLE, levels of ICs are associated with platelet activation. Because FcγRIIA is absent in mice, and murine platelets do not respond to ICs in any existing mouse model of SLE, we introduced the FcγRIIA (FCGR2A) transgene into the NZB/NZWF1 mouse model of SLE. In mice, FcγRIIA expression by bone marrow cells severely aggravated lupus nephritis and accelerated death. Lupus onset initiated major changes to the platelet transcriptome, both in FcγRIIA-expressing and nonexpressing mice, but enrichment for type I interferon response gene changes was specifically observed in the FcγRIIA mice. Moreover, circulating platelets were degranulated and were found to interact with neutrophils in FcγRIIA-expressing lupus mice. FcγRIIA expression in lupus mice also led to thrombosis in lungs and kidneys. The model recapitulates hallmarks of human SLE and can be used to identify contributions of different cellular lineages in the manifestations of SLE. The study further reveals a role for FcγRIIA in nephritis and in platelet activation in SLE.
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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.