ArticleJournal of innate immunity2014
Relative contribution of c1q and apoptotic cell-surface calreticulin to macrophage phagocytosis.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 52 citations in OpenAlex.
- The circadian gene Dec2 promotes pancreatic cancer progression and dormancy through immune evasion.Developmental cell · 2026Article
- Calreticulin-From the Endoplasmic Reticulum to the Plasma Membrane-Adventures of a Wandering Protein.Cancers · 2025Review
- Immune-mediated blood-brain barrier disruption after ischemic stroke: mechanisms and therapeutic targets.Frontiers in immunology · 2025Review
- Monocyte Production of C1q Potentiates CD8American journal of respiratory cell and molecular biology · 2024Article
- Glioblastoma Phagocytic Cell Death: Balancing the Opportunities for Therapeutic Manipulation.Cells · 2024Review
- Optical biosensor based on weak measurement for ultra-sensitive detection of calreticulin in human serum.Biomedical optics express · 2024Article
- Causal relationship between complementFrontiers in genetics · 2024Article
- Complement in Human Brain Health: Potential of Dietary Food in Relation to Neurodegenerative Diseases.Foods (Basel, Switzerland) · 2023Review
- Nanoscale imaging of CD47 informs how plasma membrane modifications shape apoptotic cell recognition.Communications biology · 2023Article
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- C1q and central nervous system disorders.Frontiers in immunology · 2023Review
- Membrane Bound CRT Fragment Accelerates Tumor Growth of Melanoma B16 Cell In Vivo through Promoting M2 Polarization via TLR4.Journal of immunology research · 2022Article
- Transient Activation of Hedgehog Signaling Inhibits Cellular Senescence and Inflammation in Radiated Swine Salivary Glands through Preserving Resident Macrophages.International journal of molecular sciences · 2021Article
- Mechanism, Prevention, and Treatment of Radiation-Induced Salivary Gland Injury Related to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2021Review
- I'm Infected, Eat Me! Innate Immunity Mediated by Live, Infected Cells Signaling To Be Phagocytosed.Infection and immunity · 2021Review
- The Phagocytic Code Regulating Phagocytosis of Mammalian Cells.Frontiers in immunology · 2021Review
- Article
- Calreticulin and cancer.Cell research · 2021Review
- Transient Activation of the Hedgehog-Gli Pathway Rescues Radiotherapy-Induced Dry Mouth via Recovering Salivary Gland Resident Macrophages.Cancer research · 2020Article
- The Interactions of Parasite Calreticulin With Initial Complement Components: Consequences in Immunity and Virulence.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q has been shown to recognize apoptotic cells, to enhance their uptake and to modulate cytokine release by phagocytes and thus promote immune tolerance. Surface-exposed calreticulin (CRT), known as a C1q receptor, is also considered to be an early eat-me signal that enhances the phagocytosis of apoptotic cells and is capable of eliciting an immunogenic response. However, the molecular mechanisms that trigger these functions are not clear. We hypothesized that CRT and C1q might act together in these processes. We first showed, by means of fluorescence resonance energy transfer (FRET), that CRT interacts with the C1q globular region at the surface of early apoptotic cells. Next, we pointed out that knockdown of CRT on early apoptotic HeLa cells impairs the enhancement effect of C1q on their uptake by THP-1 monocyte-derived macrophages. Furthermore, a deficiency of CRT induces contrasting effects on cytokine release by THP-1 macrophages, increasing interleukin (IL)-6 and monocyte chemotactic protein 1/CCL2 and decreasing IL-8. Remarkably, these effects were greatly reduced when apoptotic cells were opsonized by C1q, which counterbalanced the effect of the CRT deficiency. These results demonstrate that CRT-C1q interaction is involved in the C1q bridging function and they highlight the particular ability of C1q to control the phagocyte inflammatory status, i.e. by integrating the molecular changes that could occur at the surface of dying cells.
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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.