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Macrophage complement receptors and pathogen clearance
Open accessAbstract
Phagocytosis, an important mechanism of the host-defence system and a primary function of macrophages, is facilitated by opsonization, a process by which serum components tag pathogens for recognition by neutrophils and macrophages. Complement component C3 is central to opsonization. Its first cleavage product, C3b, forms the multisubunit enzyme, C3bBb, which proteolytically cleaves additional C3 molecules on the pathogen surface. C3b is further degraded to iC3b, C3c and C3dg, products that serve as ligands for selective complement receptors on leukocytes. This receptor-ligand interaction subsequently modulates immune responses or directly targets the pathogen for clearance by phagocytosis. Although a central role for C3 in phagocytosis of certain pathogens is well accepted, the receptors orchestrating the phagocytic response have not been well characterized. The recent structures of C3 and its breakdown products have increased our insights into the molecular basis of complement activation and recognition by their receptors. Here we review the biology of macrophage receptors for C3 fragments and discuss their role in the host response to pathogens.
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“In the immune system, C3 is cleaved into an activated form, iC3b, which covalently binds to the surface of cells or debris and targets them for elimination by macrophages via specific phagocytic receptor signaling (e.g., CR3) (Lambris and Tsokos, 1986; van Lookeren Campagne et al., 2007).”
From Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012) · cites this paper as van Lookeren Campagne et al., 2007
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“Anaphylatoxin C3a and C5a—downstream products of the complement pathway [211]—function as chemoattractants for neutrophils [212], macrophages [213], astrocytes [214], and microglia [215–217] (Fig. 4B&G).”
From Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination (2022) · cites this paper as [213]
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Metadata
- Authors
- van Lookeren Campagne, M., Wiesmann, C., & Brown, E. J.
- Affiliations
- Genentech (US)
- Venue
- Cellular Microbiology
- Publisher
- Hindawi Limited
- Published
- 2007-09
- Volume
- 9
- Issue
- 9
- Pages
- 2095-2102
- ISSN
- 1462-5814 (ISSN-L)
- 1462-5822
- OpenAlex
- W2007658022
- Cited by
- 332
- References
- 67
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 14 · 2023: 23 · 2022: 15 · 2021: 18 · 2020: 27 · 2019: 18 · 2018: 9 · 2017: 25 · 2016: 17 · 2015: 22 · 2014: 20 · 2013: 19 · 2012: 20
- FWCI
- 1.17
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cellular Microbiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Keywords
- complement C3, opsonization, phagocytosis, C3b, iC3b, C3dg, C3c, complement activation, pathogen clearance, host defense, ligand-receptor interactions
- MeSH terms
- Complement Activation, Complement C3, Macrophages, Models, Molecular, Opsonin Proteins, Phagocytosis, Protein Conformation, Receptors, Complement, Protein Isoforms
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