ArticlePLoS pathogens2010
The meningococcal vaccine candidate neisserial surface protein A (NspA) binds to factor H and enhances meningococcal resistance to complement.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 158 citations in OpenAlex.
- Review
- Identification of a Kingella kingae factor H binding protein that is the major determinant of serum resistance.PLoS pathogens · 2025Article
- Human Factor H and anti-Neisserial surface protein A (NspA) antibodies compete for overlapping binding sites on meningococcal NspA.Infection and immunity · 2025Article
- Mechanisms by which Factor H protectsFrontiers in immunology · 2024Article
- Pan-genome wide association study ofFrontiers in microbiology · 2023Article
- PathogenicInfection and immunity · 2022Article
- Variation in CFHR3 determines susceptibility to meningococcal disease by controlling factor H concentrations.American journal of human genetics · 2022Article
- The Exploration of Complement-Resistance Mechanisms of Pathogenic Gram-Negative Bacteria to Support the Development of Novel Therapeutics.Pathogens (Basel, Switzerland) · 2022Review
- Edwardsiella tarda TraT is an anti-complement factor and a cellular infection promoter.Communications biology · 2022Article
- Low Levels of Factor H Family Proteins During Meningococcal Disease Indicate Systemic Processes Rather Than Specific Depletion byFrontiers in immunology · 2022Article
- The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022Review
- Genomic analysis of Neisseria elongata isolate from a patient with infective endocarditis.FEBS open bio · 2021Article
- Two human antibodies to a meningococcal serogroup B vaccine antigen enhance binding of complement Factor H by stabilizing the Factor H binding site.PLoS pathogens · 2021Article
- Evolution of Sequence Type 4821 Clonal Complex Hyperinvasive and Quinolone-Resistant Meningococci.Emerging infectious diseases · 2021Article
- Deconvolution of intergenic polymorphisms determining high expression of Factor H binding protein in meningococcus and their association with invasive disease.PLoS pathogens · 2021Article
- Interactions Between PathogenicFrontiers in cellular and infection microbiology · 2021Review
- Factor H binding protein (fHbp)-mediated differential complement resistance of a serogroup CAccess microbiology · 2021Article
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Broad vaccine protection against Neisseria meningitidis using factor H binding protein.Vaccine · 2020Review
- Neisseria meningitidis Urethritis Outbreak Isolates Express a Novel Factor H Binding Protein Variant That Is a Potential Target of Group B-Directed Meningococcal (MenB) Vaccines.Infection and immunity · 2020Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Complement forms an important arm of innate immunity against invasive meningococcal infections. Binding of the alternative complement pathway inhibitor factor H (fH) to fH-binding protein (fHbp) is one mechanism meningococci employ to limit complement activation on the bacterial surface. fHbp is a leading vaccine candidate against group B Neisseria meningitidis. Novel mechanisms that meningococci employ to bind fH could undermine the efficacy of fHbp-based vaccines. We observed that fHbp deletion mutants of some meningococcal strains showed residual fH binding suggesting the presence of a second receptor for fH. Ligand overlay immunoblotting using membrane fractions from one such strain showed that fH bound to a approximately 17 kD protein, identified by MALDI-TOF analysis as Neisserial surface protein A (NspA), a meningococcal vaccine candidate whose function has not been defined. Deleting nspA, in the background of fHbp deletion mutants, abrogated fH binding and mAbs against NspA blocked fH binding, confirming NspA as a fH binding molecule on intact bacteria. NspA expression levels vary among strains and expression correlated with the level of fH binding; over-expressing NspA enhanced fH binding to bacteria. Progressive truncation of the heptose (Hep) I chain of lipooligosaccharide (LOS), or sialylation of lacto-N-neotetraose LOS both increased fH binding to NspA-expressing meningococci, while expression of capsule reduced fH binding to the strains tested. Similar to fHbp, binding of NspA to fH was human-specific and occurred through fH domains 6-7. Consistent with its ability to bind fH, deleting NspA increased C3 deposition and resulted in increased complement-dependent killing. Collectively, these data identify a key complement evasion mechanism with important implications for ongoing efforts to develop meningococcal vaccines that employ fHbp as one of its components.
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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.