ArticleFrontiers in immunology2020
Local and Systemic Concentrations of Pattern Recognition Receptors of the Lectin Pathway of Complement in a Cohort of Patients With Interstitial Lung Diseases.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- The Complement System and Its Role in Eosinophilic Inflammation in Respiratory Diseases.Biomedicines · 2026Review
- Single-cell transcriptomic analysis of blood and bronchoalveolar lavage fluid in progressive fibrosing interstitial lung diseases.Scientific reports · 2025Article
- Ficolin-1 ameliorates pulmonary fibrosis via directly binding to TGF-β1.Journal of translational medicine · 2024Article
- The complement cascade in lung injury and disease.Respiratory research · 2024Review
- The Role of Ficolins in Lung Injury.Journal of innate immunity · 2024Review
- Overview on the Link Between the Complement System and Auto-Immune Articular and Pulmonary Disease.Open access rheumatology : research and reviews · 2023Review
- Association of low ficolin-2 concentration in cord serum with respiratory distress syndrome in preterm newborns.Frontiers in immunology · 2023Article
- Pentraxin 3 Inhibits Complement-driven Macrophage Activation to Restrain Granuloma Formation in Sarcoidosis.American journal of respiratory and critical care medicine · 2022Article
- PTX3 in Granuloma Formation and Sarcoidosis: Helping Macrophages Accept a "Complement".American journal of respiratory and critical care medicine · 2022Article
- Altered transcription factor targeting is associated with differential peripheral blood mononuclear cell proportions in sarcoidosis.Frontiers in immunology · 2022Article
- Article
- Functional Activity of the Complement System in Hospitalized COVID-19 Patients: A Prospective Cohort Study.Frontiers in immunologyObservational
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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
Background: The role of the lectin pathway of complement in the pathogenesis of interstitial lung diseases (ILDs) is largely unknown. Pattern recognition receptors (PRR) of the lectin pathway are involved in the clearance of apoptotic cells either via activation of the complement system or as direct opsonins. As recent findings suggest a role of apoptosis in the development of pulmonary fibrosis, the influence of plasma lectins has lately been considered in various ILDs, but data on local concentrations in the lungs are lacking. This study investigated the role of mannose-binding lectin (MBL), ficolin-2 and ficolin-3 in ILD patients with a focus on idiopathic pulmonary fibrosis (IPF) and sarcoidosis. Methods: A case control study was conducted involving 80 patients with different forms of ILD as well as 40 control patients undergoing routine flexible bronchoscopy with bronchoalveolar lavage (BAL). Plasma and BAL fluid (BALF) levels of MBL, ficolin-2 and ficolin-3 as well as complement split products C4d and C5a (only in BALF) were measured by enzyme-linked immunosorbent assays. Eight single-nucleotide polymorphisms (SNPs) of MBL and ficolin-2 were determined by genotyping and tested for their association with ILDs. Results: We included 35, 35, 10, and 40 patients with sarcoidosis, idiopathic pulmonary fibrosis (IPF), other ILD, and a control group, respectively. BALF but not plasma levels of the three PRR were significantly elevated in sarcoidosis patients compared to a control group without ILD (MBL: median 66.8 vs. 24.6 ng/ml, Conclusion: This is the first study to simultaneously assess systemic and local lectin pathway protein levels in ILD patients. Our data suggest an involvement of PRR of the lectin pathway in the pathogenesis of sarcoidosis given the significantly higher BALF levels compared to a control group. Additional analyses in a larger patient cohort are required to confirm or refute a potential effect of local and/or systemic ficolin-2 levels in IPF patients.
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