ArticleFrontiers in immunology2018
Utilization of Staphylococcal Immune Evasion Protein Sbi as a Novel Vaccine Adjuvant.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mass Spectrometry-Based Analysis of Surface Proteins inJournal of proteome research · 2025Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- Article
- Novel method for detecting complement C3 deposition on Staphylococcus aureus.Scientific reports · 2022Article
- The Protease SplB of Staphylococcus aureus Targets Host Complement Components and Inhibits Complement-Mediated Bacterial Opsonophagocytosis.Journal of bacteriology · 2022Article
- Staphylococcal Complement Evasion Protein Sbi Stabilises C3d Dimers by Inducing an N-Terminal Helix Swap.Frontiers in immunology · 2022Article
- Insights Into the Structure-Function Relationships of Dimeric C3d Fragments.Frontiers in immunology · 2021Article
- Complement Evasion Strategies of Human Pathogenic Bacteria.Indian journal of microbiology · 2020Review
- Ensilication Improves the Thermal Stability of the Tuberculosis Antigen Ag85b and an Sbi-Ag85b Vaccine Conjugate.Scientific reports · 2019Article
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Authors and funding
14 authors.
Funding
Abstract
Co-ligation of the B cell antigen receptor with complement receptor 2 on B-cells via a C3d-opsonised antigen complex significantly lowers the threshold required for B cell activation. Consequently, fusions of antigens with C3d polymers have shown great potential in vaccine design. However, these linear arrays of C3d multimers do not mimic the natural opsonisation of antigens with C3d. Here we investigate the potential of using the unique complement activating characteristics of Staphylococcal immune-evasion protein Sbi to develop a pro-vaccine approach that spontaneously coats antigens with C3 degradation products in a natural way. We show that Sbi rapidly triggers the alternative complement pathway through recruitment of complement regulators, forming tripartite complexes that act as competitive antagonists of factor H, resulting in enhanced complement consumption. These functional results are corroborated by the structure of the complement activating Sbi-III-IV:C3d:FHR-1 complex. Finally, we demonstrate that Sbi, fused with
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