ArticleArthritis and rheumatism2010
Neutrophils in a mouse model of autoantibody-mediated arthritis: critical producers of Fc receptor gamma, the receptor for C5a, and lymphocyte function-associated antigen 1.
Article in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 97 citations in OpenAlex.
- Neutrophil-Linked Inflammatory Mechanisms and Biomarkers in Diabetic Microvascular Complications.Diabetes & metabolism journal · 2026Review
- The role of VISTA engagement in limiting neutrophil-mediated inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Article
- Activation of proresolving macrophages in dorsal root ganglia attenuates persistent arthritis pain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Endothelial cell sphingosine 1-phosphate receptor 1 restrains VE-cadherin cleavage and attenuates experimental inflammatory arthritis.JCI insight · 2024Article
- Infusion of GMSCs relieves autoimmune arthritis by suppressing the externalization of neutrophil extracellular traps via PGE2-PKA-ERK axis.Journal of advanced research · 2024Article
- Tissue-resident, extravascular Ly6cCell reports · 2023Article
- Modulation of Neutrophil Function by Recombinant Human IgG1 Fc Hexamer in the Endogenous K/BxN Mouse Model of Rheumatoid Arthritis.Pharmacology · 2023Article
- The selective inhibition of the Syk tyrosine kinase ameliorates experimental autoimmune arthritis.Frontiers in immunology · 2023Article
- Central Role of Semaphorin 3B in a Serum-Induced Arthritis Model and Reduced Levels in Patients With Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- Ageing and interferon gamma response drive the phenotype of neutrophils in the inflamed joint.Annals of the rheumatic diseases · 2022Article
- The Neuroimmune Interplay in Joint Pain: The Role of Macrophages.Frontiers in immunology · 2022Review
- Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021Review
- Neuronal interleukin-1 receptors mediate pain in chronic inflammatory diseases.The Journal of experimental medicine · 2020Article
- Neutrophil chemoattractant receptors in health and disease: double-edged swords.Cellular & molecular immunology · 2020Review
- IL-4 controls activated neutrophil FcγR2b expression and migration into inflamed joints.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Complement activation on neutrophils initiates endothelial adhesion and extravasation.Molecular immunology · 2019Article
- Neutrophil Recruitment: From Model Systems to Tissue-Specific Patterns.Trends in immunology · 2019Review
- Review
- A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis.Nature immunology · 2019Article
5 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
7 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveNeutrophils represent a prominent component of inflammatory joint effusions and are required for synovial inflammation in mouse models, but the mechanisms are poorly understood. In this study, we developed a system with which to test the importance of the production of specific factors by neutrophils in a mouse model of arthritis.
methodsNeutrophil-deficient Gfi-1(-/-) mice were administered sublethal doses of radiation and were then engrafted with donor bone marrow cells (BMCs), which resulted in the production of mature neutrophils within 2 weeks. By reconstituting with BMCs from mice lacking selected proinflammatory factors, we generated mice that specifically lacked these factors on their neutrophils. Arthritis was initiated by transfer of K/BxN serum to identify the role of defined neutrophil factors on the incidence and severity of arthritis.
resultsNeutrophils lacking the signaling chain of stimulatory Fc receptors (FcRgamma(-/-)) were unable to elicit arthritis, but neutrophils lacking FcgammaRIII still did so. Neutrophils lacking the chemotactic or adhesion receptor C5a receptor (C5aR) or CD11a/lymphocyte function-associated antigen 1 (LFA-1) also failed to initiate arthritis but could enter joints in which inflammation had been initiated by wild-type neutrophils. Neutrophils unable to produce interleukin-1alpha (IL-1alpha) and IL-1beta (IL-1alpha/beta(-/-)) or leukotrienes (5-lipoxygenase [5-LOX(-/-)]) produced arthritis of intermediate severity. The inability of neutrophils to make tumor necrosis factor or to express receptors for tumor necrosis factor or IL-1 had no effect on arthritis.
conclusionA novel transfer system was developed to identify neutrophil production of FcRgamma, C5aR, and CD11a/LFA-1 as critical components of autoantibody-mediated arthritis. Neutrophil production of IL-1 and leukotriene B(4) likely contributes to inflammation but is not essential. Molecular requirements for neutrophil influx into joints become more permissive after inflammation is initiated.
Indexed as
Identifiers
What OpenQuestion holds
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.