ArticleJournal of immunology (Baltimore, Md. : 1950)2009
A molecular insight into complement evasion by the staphylococcal complement inhibitor protein family.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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
46 citing papers in PubMed, 66 citations in OpenAlex.
- 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
- Biomaterial-mediated macrophage polarization remodeling and sequential regulation: a potential strategy in bone infections treatment.Bone research · 2025Review
- Reconstitution of the alternative pathway of the complement system enables rapid delineation of the mechanism of action of novel inhibitors.The Journal of biological chemistry · 2024Article
- Staphylococcal peroxidase inhibitor (SPIN): Residue-level investigation of the helical bundle domain.Archives of biochemistry and biophysics · 2024Article
- Mechanism of complement inhibition by a mosquito protein revealed through cryo-EM.Communications biology · 2024Article
- Clonal Diversity, Antibiotic Resistance, and Virulence Factor Prevalence of Community AssociatedPathogens (Basel, Switzerland) · 2023Article
- The effect ofFrontiers in immunology · 2023Review
- Forecasting Staphylococcus aureus Infections Using Genome-Wide Association Studies, Machine Learning, and Transcriptomic Approaches.mSystems · 2022Article
- Group BJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Complement component C3: A structural perspective and potential therapeutic implications.Seminars in immunology · 2022Review
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- Inhibition of the Complement Alternative Pathway by Chemically Modified DNA Aptamers That Bind with Picomolar Affinity to Factor B.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
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- Expression, purification, and characterization of a human complement component C3 analog that lacks the C-terminal C345c domain.Journal of immunological methods · 2019Article
- Staphylococcus aureus Evasion of Host Immunity in the Setting of Prosthetic Joint Infection: Biofilm and Beyond.Current reviews in musculoskeletal medicine · 2018Review
- Identification of a staphylococcal complement inhibitor with broad host specificity in equidThe Journal of biological chemistry · 2018Article
- Equine Methicillin-Resistant Sequence Type 398Frontiers in microbiology · 2018Article
- Identification of C3b-Binding Small-Molecule Complement Inhibitors Using Cheminformatics.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Structural Implications for the Formation and Function of the Complement Effector Protein iC3b.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
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Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Staphylococcus aureus possesses an impressive arsenal of complement evasion proteins that help the bacterium escape attack of the immune system. The staphylococcal complement inhibitor (SCIN) protein exhibits a particularly high potency and was previously shown to block complement by acting at the level of the C3 convertases. However, many details about the exact binding and inhibitory mechanism remained unclear. In this study, we demonstrate that SCIN directly binds with nanomolar affinity to a functionally important area of C3b that lies near the C terminus of its beta-chain. Direct competition of SCIN with factor B for C3b slightly decreased the formation of surface-bound convertase. However, the main inhibitory effect can be attributed to an entrapment of the assembled convertase in an inactive state. Whereas native C3 is still able to bind to the blocked convertase, no generation and deposition of C3b could be detected in the presence of SCIN. Furthermore, SCIN strongly competes with the binding of factor H to C3b and influences its regulatory activities: the SCIN-stabilized convertase was essentially insensitive to decay acceleration by factor H and the factor I- and H-mediated conversion of surface-bound C3b to iC3b was significantly reduced. By targeting a key area on C3b, SCIN is able to block several essential functions within the alternative pathway, which explains the high potency of the inhibitor. Our findings provide an important insight into complement evasion strategies by S. aureus and may act as a base for further functional studies.
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Registered trials
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