ArticleArthritis and rheumatism2011
Regulation of human neutrophil Fcγ receptor IIa by C5a receptor promotes inflammatory arthritis in mice.
Article in Arthritis and rheumatism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.
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Who cites it
45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.
- Fc Gamma Receptors as Regulators of Bone Destruction in Inflammatory Arthritis.Frontiers in immunology · 2021Pooled it
- Low copy number of the FCGR3B gene and rheumatoid arthritis: a case-control study and meta-analysis.Arthritis research & therapy · 2012Pooled it
- Clinical significance of circulating FcγRIIa in the prognosis of patients with metastatic non-small cell lung cancer.Journal of cancer research and clinical oncology · 2026Article
- From pathogenesis to therapeutic targeting: new insight into TAM receptors in rheumatoid arthritis.Cell & bioscience · 2025Review
- Receptor tyrosine kinases Tyro3, Axl, and Mertk differentially contribute to antibody-induced arthritis.Cell communication and signaling : CCS · 2023Article
- Investigation of anxiety sensitivity levels of cancer patients in terms of COVID-19 vaccine: a cross-sectional study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022Article
- Differential expression of C5aR1 and C5aR2 in innate and adaptive immune cells located in early skin lesions of bullous pemphigoid patients.Frontiers in immunology · 2022Article
- FcγR engagement reprograms neutrophils into antigen cross-presenting cells that elicit acquired anti-tumor immunity.Nature communications · 2021Article
- Inhibitory affinity modulation of FcγRIIA ligand binding by glycosphingolipids by inside-out signaling.Cell reports · 2021Article
- Anti-Citrullinated Protein Antibodies in Patients with Rheumatoid Arthritis: Biological Effects and Mechanisms of Immunopathogenesis.International journal of molecular sciences · 2020Review
- Paradigm Shifts in Mast Cell and Basophil Biology and Function: An Emerging View of Immune Regulation in Health and Disease.Methods in molecular biology (Clifton, N.J.) · 2020Review
- The Role of Complement in Transfusion-Related Acute Lung Injury.Transfusion medicine reviews · 2019Review
- Complement activation on neutrophils initiates endothelial adhesion and extravasation.Molecular immunology · 2019Article
- Cis interaction between sialylated FcγRIIA and the αI-domain of Mac-1 limits antibody-mediated neutrophil recruitment.Nature communications · 2018Article
- Complement in the Initiation and Evolution of Rheumatoid Arthritis.Frontiers in immunology · 2018Review
- Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases.The Journal of clinical investigation · 2017Article
- Myeloid Populations in Systemic Autoimmune Diseases.Clinical reviews in allergy & immunology · 2017Review
- Arthritis models: usefulness and interpretation.Seminars in immunopathology · 2017Review
- Megakaryocytes compensate for Kit insufficiency in murine arthritis.The Journal of clinical investigation · 2017Article
- Multiple Phenotypic Changes Define Neutrophil Priming.Frontiers in cellular and infection microbiology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveRheumatoid arthritis culminates in joint destruction that, in mouse models of disease, is supported by innate immune molecules, including Fcγ receptors (FcγR) and complement. However, these findings may not be predictive of the outcome in humans, given the structural differences between murine and human activating FcγR on neutrophils, a prominent component of joint exudates. The aim of this study was to examine the role of human neutrophil FcγRIIa in the development of arthritis and probe the underlying mechanism by which FcγRIIa initiates disease.
methodsK/BxN mouse serum transfer-induced arthritis was examined in mice expressing human FcγRIIa on neutrophils but lacking their own activating FcγR (γ-chain-deficient mice). The role of mast cells, complement (C3 and C5a), and CD18 integrins in FcγRIIa-initiated disease was examined using cell reconstitution approaches, inhibitors, and functional blocking antibodies, respectively. Crosstalk between the complement receptor C5aR and FcγRIIa on neutrophils was evaluated in vitro.
resultsThe expression of human FcγRIIa on neutrophils was sufficient to restore susceptibility to K/BxN serum-induced neutrophil recruitment, synovitis, and bone destruction in γ-chain-deficient mice. Joint inflammation was robust and proceeded even in the absence of mast cells and vascular permeability, features shown to contribute to disease in wild-type mice. Neutrophil recruitment was dependent on the presence of a CD18 integrin, lymphocyte function-associated antigen 1, and C5aR. In addition, C5aR significantly enhanced FcγRIIa-mediated phagocytosis and oxidative burst in vitro.
conclusionHuman and murine activating FcγR on neutrophils are not functionally equivalent, and in humans, they may play a primary role in arthritis. Crosstalk between neutrophil C5aR and FcγRIIa is essential for disease progression, thus highlighting a new aspect of complement during the effector phase of inflammatory arthritis.
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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.