ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Innate immune proteins C1q and mannan-binding lectin enhance clearance of atherogenic lipoproteins by human monocytes and macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Effect of Optimization of Glycaemic Control on Mannan-Binding Lectin in Type 1 Diabetes.Journal of diabetes research · 2017Trial
- Age-associated chemokine receptor expression profiles in human peripheral blood monocyte subsets predict cardiovascular disease risk.Frontiers in immunology · 2026Article
- Do microenvironmental changes in degenerative disc disease reflect in systemic circulation? A proteomic investigation.Clinical proteomics · 2025Article
- Article
- Efferocytosis in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Role of Complement in Liver Diseases.Seminars in liver disease · 2024Review
- Aberrant Lipid Metabolism and Complement Activation in Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2024Review
- The complement system in lipid-mediated pathologies.Frontiers in immunology · 2024Review
- Mannose-Binding Lectin Reduces Oxidized Low-Density Lipoprotein Induced Vascular Endothelial Cells Injury by Inhibiting LOX1-ox-LDL Binding and Modulating Autophagy.Biomedicines · 2023Article
- Complement C1q and von Willebrand factor interaction in atherosclerosis of human carotid artery.Frontiers in immunology · 2023Article
- Association of serum complement C1q with cardiovascular outcomes among patients with acute coronary syndrome undergoing percutaneous coronary intervention.Journal of geriatric cardiology : JGC · 2022Article
- Depletion of Homeostatic Antibodies against Malondialdehyde-Modified Low-Density Lipoprotein Correlates with Adverse Events in Major Vascular Surgery.Antioxidants (Basel, Switzerland) · 2022Article
- The OSE complotype and its clinical potential.Frontiers in immunology · 2022Review
- Identification and Validation of Candidate Gene Module Along With Immune Cells Infiltration Patterns in Atherosclerosis Progression to Plaque RuptureFrontiers in cardiovascular medicine · 2022Article
- Extracellular signal-regulated kinase 1/2 is required for complement component C1q and fibronectin dependent enhancement of Fcγ- receptor mediated phagocytosis in mouse and human cells.BMC immunology · 2020Article
- Urinary phosphate-containing nanoparticle contributes to inflammation and kidney injury in a salt-sensitive hypertension rat model.Communications biology · 2020Article
- Recombinant C1q variants modulate macrophage responses but do not activate the classical complement pathway.Molecular immunology · 2020Article
- Glucan and Mannan-Two Peas in a Pod.International journal of molecular sciences · 2019Review
- Binding of von Willebrand Factor to Complement C1q Decreases the Phagocytosis of Cholesterol Crystals and Subsequent IL-1 Secretion in Macrophages.Frontiers in immunology · 2019Article
- Cardiovascular risk and mannose binding lectin in patients with rheumatoid arthritis from southern Brazil.International journal of cardiology. Heart & vasculature · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerosis is a chronic inflammatory disorder that is characterized by the accumulation of modified lipoproteins in the arterial intima. C1q and mannan-binding lectin (MBL) are not only recognition components involved in activation of inflammation via the complement cascade, but they are also able to directly modulate phagocyte activation. Studies in C1q(-/-) and MBL(-/-) mice suggest that these molecules play a protective role in the early atherosclerotic lesion in the absence of, or prior to, expression of other complement components. However, in later stages, complement activation becomes an inappropriate inflammatory response, contributing to disease pathology. Therefore, to investigate possible molecular interactions of C1q and MBL in atherosclerotic lesions, we examined the influence of C1q and MBL in the clearance of native and modified lipoproteins by human monocytes and monocyte-derived macrophages. Both C1q and MBL are shown to bind and enhance the monocyte/monocyte-derived macrophage clearance of modified forms of low-density lipoprotein (LDL), including oxidized LDL and acetylated LDL, but not native LDL. Modified forms of LDL activate the classical complement pathway, but no lectin pathway activation was detected. Interestingly, monocytes that ingested modified LDL in the presence of C1q or MBL upregulated surface CD80 and CD31, as well as CCL2 chemokine gene expression. However, C1q and MBL also significantly reduced levels of free cholesterol accumulation in monocytes and human monocyte-derived macrophages that ingested oxidized LDL, while enhancing high-density lipoprotein-specific cholesterol efflux from these cells. These results suggest a novel pathway in which C1q and MBL influence removal and metabolism of atherogenic forms of LDL in the early stages of atherosclerosis.
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