ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Cutting edge: members of the Staphylococcus aureus extracellular fibrinogen-binding protein family inhibit the interaction of C3d with complement receptor 2.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Antibodies to coagulase ofFrontiers in immunology · 2023Article
- Staphylococcal Complement Evasion Protein Sbi Stabilises C3d Dimers by Inducing an N-Terminal Helix Swap.Frontiers in immunology · 2022Article
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
- 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
- DHX37 Impacts Prognosis of Hepatocellular Carcinoma and Lung Adenocarcinoma through Immune Infiltration.Journal of immunology research · 2020Article
- The Streptococcus agalactiae complement interfering protein combines multiple complement-inhibitory mechanisms by interacting with both C4 and C3 ligands.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- Staphylococcus aureus in the Intensive Care Unit: Are These Golden Grapes Ripe for a New Approach?The Journal of infectious diseases · 2017Review
- Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria.PloS one · 2017Article
- Let's Tie the Knot: Marriage of Complement and Adaptive Immunity in Pathogen Evasion, for Better or Worse.Frontiers in microbiology · 2017Review
- Complement component C3 - The "Swiss Army Knife" of innate immunity and host defense.Immunological reviews · 2016Review
- Interaction of Staphylococci with Human B cells.PloS one · 2016Article
- Article
- Draft Genome Sequence of Methicillin-Resistant Staphylococcus aureus Strain SA16, Representative of an Endemic Clone from a Brazilian Hospital.Genome announcements · 2013Article
- Molecular characterization of endocarditis-associated Staphylococcus aureus.Journal of clinical microbiology · 2013Article
- A structurally dynamic N-terminal helix is a key functional determinant in staphylococcal complement inhibitor (SCIN) proteins.The Journal of biological chemistry · 2013Article
- Manipulating the mediator: modulation of the alternative complement pathway C3 convertase in health, disease and therapy.Immunobiology · 2012Review
- Regulation of humoral immunity by complement.Immunity · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Staphylococcus aureus expresses a highly diversified arsenal of immune evasion proteins, many of which target the complement system. The extracellular fibrinogen-binding protein (Efb) and the Efb homologous protein (Ehp) have previously been demonstrated to bind to C3 and inhibit complement activation and amplification. In this study we present the first evidence that Efb and Ehp are also capable of inhibiting the interaction of C3d with complement receptor 2 (CR2), which plays an important role in B cell activation and maturation. The C-terminal domain of Efb efficiently blocked this interaction both in surface plasmon resonance-based competition studies and cellular assays and prevented the CR2-mediated stimulation of B cells. Furthermore, analyses of the available structural data were consistent with a molecular mechanism that reflects both steric and electrostatic effects on the C3d-CR2 interaction. Our study therefore suggests that S. aureus may disrupt both the innate and adaptive immune responses with a single protein module.
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Registered trials
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.