ArticleRheumatology (Oxford, England)2023
Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica.
Article in Rheumatology (Oxford, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Synovial microenvironment and fluorescence imaging for early rheumatoid arthritis diagnosis.Journal of pharmaceutical analysis · 2026Review
- Assessing disease activity in polymyalgia rheumatica using the systemic immune-inflammation index: A retrospective cross-sectional study.Clinical rheumatology · 2026Article
- Time to remission and steroid doses in older and younger patients with polymyalgia rheumatica.European geriatric medicine · 2026Article
- Late-Onset Spondyloarthritis Presenting as Glucocorticoid-Resistant Polymyalgia Rheumatica: A Hitherto Underappreciated Entity in Which Tumor Necrosis Factor or Interleukin -17 Blockade May Have a Therapeutic Role.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Neutrophil activation in juvenile dermatomyositis: associations with muscle function and disease progression.Pediatric rheumatology online journal · 2025Article
- Current Insights and Future Perspectives for the Use of Serological Biomarkers in Polymyalgia Rheumatica.Journal of inflammation research · 2025Review
- Synthetic polypeptides inhibit nucleic acid-induced inflammation in autoimmune diseases by disrupting multivalent TLR9 binding to LL37-DNA bundles.Nature nanotechnology · 2024Article
- Immune complexes-mediated activation of neutrophils in systemic lupus erythematosus is dependent on RNA recognition by toll-like receptor 8.Frontiers in immunology · 2024Article
- Mitochondrial N-formyl methionine peptides contribute to exaggerated neutrophil activation in patients with COVID-19.Virulence · 2023Article
- Biomarkers in the era of targeted therapy in giant cell arteritis and polymyalgia rheumatica: is it possible to replace acute-phase reactants?Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveNeutrophils are important in host defence. However, neutrophils are also linked to inflammation and organ damage. The purpose of this study was to assess whether markers of neutrophil activation are increased in PMR.
methodsLevels of immune complexes (IC), calprotectin and neutrophil extracellular traps (NETs) were measured in plasma of healthy individuals (n = 30) and patients with PMR (n = 60), at flare and upon treatment with glucocorticoids using ELISA. Plasma-mediated neutrophil activation was assessed in presence of an FcγRIIA inhibitory antibody (IV.3).
resultsPlasma levels of calprotectin and NETs were elevated in PMR (P < 0.001). Mechanistically, neutrophil activation was driven by ICs, present in plasma, able to up-regulate neutrophil activation markers CD66b and CD11b (P < 0.0001) in an FcγRIIA-dependent manner (P < 0.01). Of note, circulating levels of IC correlated with plasma induced CD66b and CD11b (r = 0.51, P = 0.004, and r = 0.46, P = 0.01, respectively) and decreased after glucocorticoid therapy. In contrast to NETs, calprotectin significantly decreased after glucocorticoid therapy (P < 0.001) and was higher in PMR without overlapping GCA compared with patients with overlapping disease (P = 0.014). Interestingly, musculoskeletal involvement was associated with elevated levels of calprotectin before initiation of glucocorticoid therapy (P = 0.036).
conclusionsNeutrophil activation, including NET formation, is increased in PMR, through IC-mediated engagement of FcγRIIA. Clinically, neutrophil activation is associated with musculoskeletal involvement, with calprotectin, but not NETs, being a biomarker of treatment response in PMR patients. In all, IC-mediated neutrophil activation is a central process in PMR pathogenesis identifying potential novel therapeutic targets (FcγRIIA), as well as soluble markers for disease monitoring (calprotectin).
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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.