ArticleArthritis research & therapy2012
C5a and its receptors in human anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
Article in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- The alternative complement pathway in ANCA-associated vasculitis: further evidence and a meta-analysis.Clinical and experimental immunology · 2020Pooled it
- Urinary complement C3 fragment levels and their clinical relevance in MPO-ANCA-associated vasculitis.Scientific reports · 2026Article
- Novel Treatment Paradigms: Complement Inhibition in Antineutrophil Cytoplasmic Autoantibody Vasculitis.Kidney international reports · 2025Review
- The Influence of Anti-C3aR and Anti-C5aR Antibody Levels on the Course of Specific Glomerulonephritis Types.Journal of clinical medicine · 2025Article
- Avacopan is effective in inducing remission for MPA/GPA, regardless of changes in serum C5a levels: a single-center study in Japan.BMC rheumatology · 2025Article
- Neutrophils and Platelets as Key Players in the Pathogenesis of ANCA-Associated Vasculitis and Potential Sources of Disease Activity Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Evaluating the usefulness of C5 and C5AR1 as genetic biomarkers of IgA-mediated vasculitis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Biomarkers in ANCA associated vasculitis: clinical utility, pitfalls and their role in the outcomes assessment.Frontiers in immunology · 2025Review
- Regulatory T cell therapy for myeloperoxidase-specific anti-neutrophil cytoplasmic antibody associated vasculitis.Frontiers in immunology · 2025Review
- Complement as a major mediator of ANCA vasculitis and a target for precision therapy.Expert review of clinical immunology · 2025Review
- Dapsone Alters Phenotypical and Functional Properties of Human Neutrophils In Vitro.Molecules (Basel, Switzerland) · 2024Article
- Pathogenesis of Pulmonary Manifestations in ANCA-Associated Vasculitis and Goodpasture Syndrome.International journal of molecular sciences · 2024Review
- Non-Invasive Biomarkers for Diagnosis, Risk Prediction, and Therapy Guidance of Glomerular Kidney Diseases: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Urinary complement biomarkers in immune-mediated kidney diseases.Frontiers in immunology · 2024Review
- The role of complement in kidney disease.Nature reviews. Nephrology · 2023Review
- Neutrophil extracellular trap formation in anti-neutrophil cytoplasmic antibody-associated and large-vessel vasculitis.Clinical immunology (Orlando, Fla.) · 2023Article
- Article
- The complement system and autoimmune diseases.Chronic diseases and translational medicine · 2022Review
- Neutrophil activation in patients with anti-neutrophil cytoplasmic autoantibody-associated vasculitis and large-vessel vasculitis.Arthritis research & therapy · 2022Article
- Accumulation of CytochromeInternational journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe complement system is crucial for the development of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). In particular, C5a plays a central role. In this study, plasma and urinary levels of C5a as well as renal C5a receptors (CD88 and C5L2) expression were investigated in patients with AAV.
methodsTwenty-four patients with AAV in the active phase, 19 patients with AAV in the remission phase, and 20 patients with lupus nephritis (LN) were included. Plasma and urinary levels of C5a were measured with enzyme-linked immunosorbent assay (ELISA). The staining of CD88 and C5L2 in renal specimens was detected with immunohistochemistry.
resultsThe level of plasma C5a was significantly higher in patients with AAV in the active phase than that in patients in remission, that in patients with LN, and that in normal controls. The urinary C5a level was significantly higher in patients with AAV in the active phase than that in patients in remission and that in normal controls, but not significantly different between patients with active AAV and patients with LN. The mean optical density of CD88 staining in the tubulointerstitium was significantly lower in AAV patients than that in normal controls (0.0052 ± 0.0011 versus 0.029 ± 0.0042; P = 0.005). The mean optical density of C5L2 in glomeruli was significantly higher in AAV patients than that in normal controls (0.013 ± 0.0027 versus 0.0032 ± 0.0006; P < 0.001). The mean optical density of CD88 staining closely correlated with the initial eGFR (r = 0.835; P < 0.001) in AAV patients. Double-labeling immunofluorescence assay suggested that CD88 did not express on neutrophils, monocytes, or macrophages, but C5L2 expressed on neutrophils (or monocytes) and macrophages.
conclusionThe elevated plasma and urinary C5a levels indicated complement activation in human AAV. The level of renal CD88 expression could reflect the disease severity of ANCA-associated glomerulonephritis. CD88 expression was downregulated, and C5L2 was upregulated in ANCA-associated glomerulonephritis.
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