ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Complement component C1q regulates macrophage expression of Mer tyrosine kinase to promote clearance of apoptotic cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
57 citing papers in PubMed, 78 citations in OpenAlex.
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- Spatial transcriptomic analyses highlight distinct erythroid niches in mice and humans.Nature genetics · 2026Article
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Collagen binding adhesin restricts Staphylococcus aureus skin infection.Nature communications · 2026Article
- Proteolytic dysfunction in bovine digital dermatitis caused by Treponema spp. and the therapeutic use of non-antimicrobial matrix metalloproteinase inhibitors.Communications biology · 2025Article
- Characteristics of glomerulonephritis with dominant C1q precipitation compared to corresponding glomerulonephritis without C1q staining on immunofluorescent examination.Kidney research and clinical practice · 2025Article
- Transcriptomic characterization of human pancreatic CD206- and CD206 + macrophages.Scientific reports · 2025Article
- Efferocytosis: The Janus-Faced Gatekeeper of Aging and Tumor Fate.Aging cell · 2025Review
- Integrative analyses of bulk and single-cell RNA-seq reveals the correlation between SPP1Cancer immunology, immunotherapy : CII · 2024Article
- Review
- The chromatin landscape of pathogenic transcriptional cell states in rheumatoid arthritis.Nature communications · 2024Article
- Septic macrophages induce T cells immunosuppression in a cell-cell contact manner with the involvement of CR3.Heliyon · 2024Article
- Single-nuclei transcriptome analysis of channel catfish spleen provides insight into the immunome of an aquaculture-relevant species.PloS one · 2024Article
- CXAmerican journal of respiratory and critical care medicine · 2023Article
- The Chromatin Landscape of Pathogenic Transcriptional Cell States in Rheumatoid Arthritis.bioRxiv : the preprint server for biology · 2023Article
- The immunogenic radiation and new players in immunotherapy and targeted therapy for head and neck cancer.Frontiers in oral health · 2023Review
- Editorial: The key role of Mer receptor tyrosine kinase: where inflammation ends and fibrosis begins.Frontiers in immunology · 2023Article
- Understanding the contextual functions of C1q and LAIR-1 and their applications.Experimental & molecular medicine · 2022Review
- The TAM receptor tyrosine kinases Axl and Mer drive the maintenance of highly phagocytic macrophages.Frontiers in immunology · 2022Article
- Emerging Role of C5 Complement Pathway in Peripheral Neuropathies: Current Treatments and Future Perspectives.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Failure to efficiently clear apoptotic cells is linked to defects in development and the onset of autoimmunity. Complement component C1q is required for efficient engulfment of apoptotic cells in mice and humans; however, the molecular mechanisms leading to C1q-dependent engulfment are not fully understood. In this study, we used primary mouse macrophages to identify and characterize a novel molecular mechanism for macrophage-mediated C1q-dependent engulfment of apoptotic cells. We found that macrophage activation with C1q resulted in cycloheximide-sensitive enhanced engulfment, indicating a requirement for de novo protein synthesis. To investigate the cycloheximide-sensitive pathway, C1q-elicited macrophage transcripts were identified by microarray. C1q triggered the expression of Mer tyrosine kinase (Mer) and the Mer ligand growth arrest-specific 6: a receptor-ligand pair that mediates clearance of apoptotic cells. Full-length native C1q, and not the collagen-like tail or heat-denatured protein, stimulated Mer expression. This novel pathway is specific to C1q because mannose-binding lectin, a related collectin, failed to upregulate Mer expression and function. Soluble Mer-Fc fusion protein inhibited C1q-dependent engulfment of apoptotic cells, indicating a requirement for Mer. Moreover, Mer-deficient macrophages failed to respond to C1q with enhanced engulfment. Our results suggest that C1q elicits a macrophage phenotype specifically tailored for apoptotic cell clearance, and these data are consistent with the established requirement for C1q in prevention of autoimmunity.
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Registered trials
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.