ArticleProceedings of the National Academy of Sciences of the United States of America2012
Neutrophils orchestrate their own recruitment in murine arthritis through C5aR and FcγR signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
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Who cites it
75 citing papers in PubMed, 130 citations in OpenAlex.
- Phase I Studies of Acebilustat: Biomarker Response and Safety in Patients with Cystic Fibrosis.Clinical and translational science · 2017Trial
- Review
- The receptor BLT1 is essential on neutrophils in a mouse model of mucous membrane pemphigoid.JCI insight · 2025Article
- Article
- Biomaterials for Modulating the Immune Microenvironment in Rheumatoid Arthritis.BME frontiers · 2025Review
- An Intriguing Structural Modification in Neutrophil Migration Across Blood Vessels to Inflammatory Sites: Progress in the Core Mechanisms.Cell biochemistry and biophysics · 2024Review
- Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity.Cells · 2023Review
- A subset of type-II collagen-binding antibodies prevents experimental arthritis by inhibiting FCGR3 signaling in neutrophils.Nature communications · 2023Article
- Eculizumab treatment alters the proteometabolome beyond the inhibition of complement.JCI insight · 2023Article
- C5aR1 signaling triggers lung immunopathology in COVID-19 through neutrophil extracellular traps.The Journal of clinical investigation · 2023Article
- Neutrophil-activating therapy for the treatment of cancer.Cancer cell · 2023Article
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Modulation of Neutrophil Function by Recombinant Human IgG1 Fc Hexamer in the Endogenous K/BxN Mouse Model of Rheumatoid Arthritis.Pharmacology · 2023Article
- Monocyte populations are involved in the pathogenesis of experimental epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Nonhematopoietic IRAK1 drives arthritis via neutrophil chemoattractants.JCI insight · 2022Article
- G-Protein-Coupled Receptors in Rheumatoid Arthritis: Recent Insights into Mechanisms and Functional Roles.Frontiers in immunology · 2022Review
- Heterogeneity of neutrophils and inflammatory responses in patients with COVID-19 and healthy controls.Frontiers in immunology · 2022Article
- The Neuroimmune Interplay in Joint Pain: The Role of Macrophages.Frontiers in immunology · 2022Review
- Neutrophils: Amoeboid Migration and Swarming Dynamics in Tissues.Frontiers in cell and developmental biology · 2022Review
- Crosstalk between B cells and neutrophils in rheumatoid arthritis.Immunology · 2021Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Neutrophil recruitment into the joint is a hallmark of inflammatory arthritides, including rheumatoid arthritis (RA). In a mouse model of autoantibody-induced inflammatory arthritis, neutrophils infiltrate the joint via multiple chemoattractant receptors, including the leukotriene B(4) (LTB(4)) receptor BLT1 and the chemokine receptors CCR1 and CXCR2. Once in the joint, neutrophils perpetuate their own recruitment by releasing LTB(4) and IL-1β, presumably after activation by immune complexes deposited on joint structures. Two pathways by which immune complexes may activate neutrophils include complement fixation, resulting in the generation of C5a, and direct engagement of Fcγ receptors (FcγRs). Previous investigations showed that this model of autoantibody-induced arthritis requires the C5a receptor C5aR and FcγRs, but the simultaneous necessity for both pathways was not understood. Here we show that C5aR and FcγRs work in sequence to initiate and sustain neutrophil recruitment in vivo. Specifically, C5aR activation of neutrophils is required for LTB(4) release and early neutrophil recruitment into the joint, whereas FcγR engagement upon neutrophils induces IL-1β release and subsequent neutrophil-active chemokine production, ensuring continued inflammation. These findings support the concept that immune complex-mediated leukocyte activation is not composed of overlapping and redundant pathways, but that each element serves a distinct and critical function in vivo, culminating in tissue inflammation.
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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.