ArticleArthritis & rheumatology (Hoboken, N.J.)2023
Combination of Two Monoclonal Anti-Citrullinated Protein Antibodies Induced Tenosynovitis, Pain, and Bone Loss in Mice in a Peptidyl Arginine Deiminase-4-Dependent Manner.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 29 citations in OpenAlex.
- Anti-Modified Protein Antibodies in Rheumatoid Arthritis: Pathogenic, Protective, or Passive Bystander?Immunological reviews · 2026Review
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- TNF-α blockade with adalimumab restores bone metabolism in rheumatoid arthritis by regulating cytokines and inflammatory cell infiltration.Frontiers in immunology · 2026Article
- Pain in systemic lupus erythematosus: emerging insights and paradigms.Nature reviews. Rheumatology · 2025Review
- Recognition of Glycine Versus Nonglycine Citrulline Motifs Dictating the HLA Class II Association of Anticitrullinated Protein Antibodies: Insights From Autoantibody Profiling of 6,900 Scandinavian Patients With Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Anti-Peptidylarginine Deiminase 4 Autoantibodies Derived From Patients With Rheumatoid Arthritis Exert Pathogenic Effects by Activating Monocytes and Exacerbating Inflammatory Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Citrullinated peptides as drug candidates for rheumatoid arthritis.Frontiers in immunology · 2025Review
- Identification of early risk factors for anti-citrullinated-protein-antibody positive rheumatoid arthritis-a prospective cohort study.Rheumatology (Oxford, England) · 2024Article
- The role of anti-citrullinated protein antibody in pathogenesis of RA.Clinical and experimental medicine · 2024Review
- The peculiar features, diversity and impact of citrulline-reactive autoantibodies.Nature reviews. Rheumatology · 2024Review
- Neutrophils in Inflammatory Bone Diseases.Current osteoporosis reports · 2024Review
- Anti-cyclic citrullinated peptide antibody and pain sensitisation in patients with rheumatoid arthritis: a cross-sectional analysis.Annals of the rheumatic diseases · 2023Article
- Divergent and dominant anti-inflammatory effects of patient-derived anticitrullinated protein antibodies (ACPA) in arthritis development.Annals of the rheumatic diseases · 2023Article
- Anti-Citrullinated Protein Antibody Reactivity towards Neutrophil-Derived Antigens: Clonal Diversity and Inter-Individual Variation.Biomolecules · 2023Article
- Prevention vs treatment of rheumatoid arthritis.Immunotherapy advances · 2023Review
- Role and Therapeutic Targeting Strategies of Neutrophil Extracellular Traps in Inflammation.International journal of nanomedicine · 2023Review
- Precision medicine: the precision gap in rheumatic disease.Nature reviews. Rheumatology · 2022Review
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe appearance of anti-citrullinated protein antibodies (ACPAs) in the circulation represents a major risk factor for developing rheumatoid arthritis (RA). Patient-derived ACPAs have been shown to induce pain and bone erosion in mice, suggesting an active role in the pathogenicity of RA. We undertook this study to investigate whether ACPAs can induce tenosynovitis, an early sign of RA, in addition to pain and bone loss and whether these symptoms are dependent on peptidyl arginine deiminase 4 (PAD4).
methodsMonoclonal ACPAs generated from plasma cells of RA patients were transferred to wild-type and PAD4-deficient mice. Pain-like behavior and macroscopic inflammation were monitored for a period of 4 weeks, followed by the analyses of tenosynovitis in the ankle joints using magnetic resonance imaging (MRI) and bone microarchitecture in the tibia using an X-ray microscope. Microscopic changes in the tendon sheath were analyzed in decalcified ankle joint sections.
resultsThe combination of 2 monoclonal ACPAs (1325:04C03 and 1325:01B09) induced long-lasting pain-like behavior and trabecular bone loss in mice. Although no synovitis was observed macroscopically, we detected tenosynovitis in the ACPA-injected mice by MRI. Microscopic analyses of the joints revealed a cellular hyperplasia and a consequent enlargement of the tendon sheath in the ACPA-treated group. In PAD4
conclusionMonoclonal ACPAs can induce tenosynovitis in addition to pain and bone loss via mechanisms dependent on PAD4-mediated citrullination.
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