ArticleNature2006
Structure of C3b in complex with CRIg gives insights into regulation of complement activation.
Article in Nature, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed, 241 citations in OpenAlex.
- Complement-mediated opsonization of invasive group A Streptococcus pyogenes strain AP53 is regulated by the bacterial two-component cluster of virulence responder/sensor (CovRS) system.The Journal of biological chemistry · 2013Trial
- VSIG4 Inhibits Microglia-Mediated Neuroinflammation and Neuronal Injury by Modulating the JAK2-STAT3/NF-κB Signaling Pathway in Parkinson's Disease.Molecular neurobiology · 2026Article
- Bifidobacterium bifidum-derived nanoparticles attenuate alcoholic liver disease via enhanced hepatic phagocytosis and gastrointestinal homeostasis.Nature communications · 2026Article
- The C-terminal domain of Staphylococcus aureus Efb recruits FHR-2 to C3b, synergistically inhibiting the terminal complement pathway.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Dynamic expression of complement receptor immunoglobulin (CRIg) on monocytes and its role in phagocytosis and killing of Staphylococcus aureus.Journal of biomedical science · 2026Article
- Structural insights into C3 convertase activity of the classical pathway of complement.Nature communications · 2025Article
- VSIG4 Is Dispensable for Tumor Growth and Metastasis in Murine Colorectal and Breast Cancer Models.Cancers · 2025Article
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- The Complement System.Advances in experimental medicine and biology · 2025Review
- A novel and rapid method to purify the human complement opsonin C3b from human plasma.Frontiers in immunology · 2025Article
- CG001, a C3b-targeted complement inhibitor, blocks 3 complement pathways: development and preclinical evaluation.Blood advances · 2024Article
- Antibodies Targeting Human or Mouse VSIG4 Repolarize Tumor-Associated Macrophages Providing the Potential of Potent and Specific Clinical Anti-Tumor Response Induced across Multiple Cancer Types.International journal of molecular sciences · 2024Article
- Mechanism of complement inhibition by a mosquito protein revealed through cryo-EM.Communications biology · 2024Article
- Article
- New Insights into the Complement Receptor of the Ig Superfamily Obtained from Structural and Functional Studies on Two Mutants.ImmunoHorizons · 2023Article
- Transcriptomics unveils immune metabolic disruption and a novel biomarker of mortality in patients with HBV-related acute-on-chronic liver failure.JHEP reports : innovation in hepatology · 2023Article
- Mutations from patients with IPEX ported to mice reveal different patterns of FoxP3 and Treg dysfunction.Cell reports · 2023Article
- VSIG4 interaction with heparan sulfates inhibits VSIG4-complement binding.Glycobiology · 2023Article
- Structural biology of complement receptors.Frontiers in immunology · 2023Review
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
65 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is a key part of the innate immune system, and is required for clearance of pathogens from the bloodstream. After exposure to pathogens, the third component of the complement system, C3, is cleaved to C3b which, after recruitment of factor B, initiates formation of the alternative pathway convertases. CRIg, a complement receptor expressed on macrophages, binds to C3b and iC3b mediating phagocytosis of the particles, but it is unknown how CRIg selectively recognizes proteolytic C3-fragments and whether binding of CRIg to C3b inhibits convertase activation. Here we present the crystal structure of C3b in complex with CRIg and, using CRIg mutants, provide evidence that CRIg acts as an inhibitor of the alternative pathway of complement. The structure shows that activation of C3 induces major structural rearrangements, including a dramatic movement (>80 A) of the thioester-bond-containing domain through which C3b attaches to pathogen surfaces. We show that CRIg is not only a phagocytic receptor, but also a potent inhibitor of the alternative pathway convertases. The structure provides insights into the complex macromolecular structural rearrangements that occur during complement activation and inhibition. Moreover, our structure-function studies relating the structural basis of complement activation and the means by which CRIg inhibits the convertases provide important clues to the development of therapeutics that target complement.
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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.