ArticleScientific reports2017
Cytokines regulate complement receptor immunoglobulin expression and phagocytosis of Candida albicans in human macrophages: A control point in anti-microbial immunity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- The Key Role of Complement Receptor CRIg in Kupffer Cell-Mediated Liver Disease Progression.Viruses · 2026Review
- Dynamic expression of complement receptor immunoglobulin (CRIg) on monocytes and its role in phagocytosis and killing of Staphylococcus aureus.Journal of biomedical science · 2026Article
- Targeting Virulence Factors ofFoods (Basel, Switzerland) · 2022Review
- Neutrophils Require Activation to Express Functional Cell-Surface Complement Receptor Immunoglobulin.Frontiers in immunology · 2022Article
- V-Set and immunoglobulin domain containing (VSIG) proteins as emerging immune checkpoint targets for cancer immunotherapy.Frontiers in immunology · 2022Review
- Conserved and Distinct Elements of Phagocytosis in Human andInternational journal of molecular sciences · 2021Review
- Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens.Communications biology · 2021Article
- Synthetic Naphthofuranquinone Derivatives Are Effective in Eliminating Drug-ResistantFrontiers in microbiology · 2020Article
- Less IgA deposits with more severe disease: the immunoclinical paradox in Henoch-Schönlein Purpura with MEFV mutations.Clinical rheumatology · 2019Article
- Human Dendritic Cells Express the Complement Receptor Immunoglobulin Which Regulates T Cell Responses.Frontiers in immunology · 2019Article
Corrections and comments
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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
Complement Receptor Immunoglobulin (CRIg), selectively expressed by macrophages, plays an important role in innate immunity by promoting phagocytosis of bacteria. Thus modulation of CRIg on macrophages by cytokines can be an important mechanism by which cytokines regulate anti-microbial immunity. The effects of the cytokines, tumor necrosis factor, transforming growth factor-β1, interferon-γ, interleukin (IL)-4, IL-13, IL-10, IL-1β, IL-6, lymphotoxin-α, macrophage-colony stimulating factor (M-CSF) and GM-CSF on CRIg expression were examined in human macrophages. We demonstrated that cytokines regulated the CRIg expression on macrophages during their development from monocytes in culture at the transcriptional level using qPCR and protein by Western blotting. Both CRIg spliced forms (Long and Short), were similarly regulated by cytokines. Direct addition of cytokines to matured CRIg+ macrophages also changed CRIg mRNA expression, suggesting that cytokines control macrophage function via CRIg, at two checkpoints. Interestingly the classical complement receptors, CR3 and CR4 were differentially regulated by cytokines. The changes in CRIg but not CR3/CR4 mRNA expression correlated with ability to phagocytose Candida albicans by macrophages. These findings suggest that CRIg is likely to be a control point in infection and immunity through which cytokines can mediate their effects, and is differentially regulated from CR3 and CR4 by cytokines.
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