Observational studyArthritis research & therapy2019
Role of lectin pathway complement proteins and genetic variants in organ damage and disease severity of systemic sclerosis: a cross-sectional study.
Observational study in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Anti-RNA polymerase III antibodies in systemic sclerosis: prevalence and clinical associations from a systematic review and meta-analysis.Rheumatology (Oxford, England) · 2025Pooled it
- Ficolin-1 ameliorates pulmonary fibrosis via directly binding to TGF-β1.Journal of translational medicine · 2024Article
- Disturbed Complement Receptor Expression Pattern of B Cells Is Enhanced by Toll-like Receptor CD180 Ligation in Diffuse Cutaneous Systemic Sclerosis.International journal of molecular sciences · 2024Article
- The Role of Ficolins in Lung Injury.Journal of innate immunity · 2024Review
- Biomarkers in the Pathogenesis, Diagnosis, and Treatment of Systemic Sclerosis.Journal of inflammation research · 2023Review
- Increased Complement Activation in Systemic Sclerosis Patients with Skin and Lung Fibrosis.Journal of personalized medicine · 2022Article
- Article
- Beyond Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome: The Relevance of Complement From Pathogenesis to Pregnancy Outcome in Other Systemic Rheumatologic Diseases.Frontiers in pharmacology · 2022Review
- Local and Systemic Concentrations of Pattern Recognition Receptors of the Lectin Pathway of Complement in a Cohort of Patients With Interstitial Lung Diseases.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of the complement system in the pathogenesis of systemic sclerosis (SSc) is controversial. This study investigated the role of the lectin pathway of complement as a mediator of ischemia/reperfusion injury in SSc.
methodsThis is a prospective observational cross-sectional study of 211 SSc patients and 29 patients with Raynaud's phenomenon in undifferentiated connective tissue disease (UCTD) at risk of developing SSc from two outpatient clinics. Serum levels of lectin pathway proteins (FCN-2, FCN-3, MBL, and MASP-2) and eight MBL2 and FCN2 single-nucleotide polymorphisms (SNP) were analyzed by sandwich-type immunoassays and genotyping and examined for their association with disease manifestations.
resultsLectin pathway protein levels and SNPs were similar between SSc and UCTD patients. FCN-2 levels were however higher in SSc patients with present evidence of digital ulcers (mean 1.4 vs. 1.0 μg/mL, p = 0.05), pitting scars (mean 1.3 vs. 1.0 μg/mL, p = 0.01), and puffy fingers (mean 1.2 vs. 1.0 μg/mL, p = 0.04). Similarly, higher FCN-2 levels were observed in SSc patients with Scl-70 autoantibodies (mean 1.5 vs. 1.0 μg/mL, p = 0.001), interstitial lung disease (mean 1.2 vs. 0.9 μg/mL, p = 0.02), and a forced vital capacity (FVC) below 80% (mean 1.4 vs. 1.0 μg/mL, p = 0.02). In line, variant alleles in the FCN-2 SNP at position + 6359 were associated with a significantly reduced FVC and diffusion capacity. Furthermore, patients with SSc renal crisis harbored higher MBL levels (mean 2.7 vs. 1.5 μg/mL, p = 0.04). No other lectin pathway protein levels or polymorphisms were associated with disease manifestations, low complement C3 and/or C4 levels, or inflammatory markers.
conclusionsThis study does not support a relevant role for several lectin pathway complement proteins in the pathogenesis of SSc. Higher FCN-2 levels were however associated with Scl-70 autoantibody positivity, interstitial lung involvement, and digital vasculopathy. Elevated MBL levels were associated with renal crisis.
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