ArticleeLife2014
Competition between antagonistic complement factors for a single protein on N. meningitidis rules disease susceptibility.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Identification of novel blood-borne soluble binding partners of factor H-related proteins.Scientific reports · 2026Article
- Functional and structural characterization of mouse Factor H-related B protein unveils a novel dimerization domain shared by FHR-B and FH.Frontiers in immunology · 2025Article
- Role of factor H-related protein 3 inFrontiers in immunology · 2024Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- Meningococcal factor H-binding protein: implications for disease susceptibility, virulence, and vaccines.Trends in microbiology · 2023Review
- The Factor H protein family: The switchers of the complement alternative pathway.Immunological reviews · 2023Review
- Plasma proteomic profiling of bacterial cold water disease-resistant and -susceptible rainbow trout lines and biomarker discovery.Frontiers in immunology · 2023Article
- Genetic variability shapes the alternative pathway complement activity and predisposition to complement-related diseases.Immunological reviews · 2023Review
- PathogenicInfection and immunity · 2022Article
- Variation in CFHR3 determines susceptibility to meningococcal disease by controlling factor H concentrations.American journal of human genetics · 2022Article
- Low Levels of Factor H Family Proteins During Meningococcal Disease Indicate Systemic Processes Rather Than Specific Depletion byFrontiers in immunology · 2022Article
- Genome-wide association studies reveal the role of polymorphisms affecting factor H binding protein expression in host invasion by Neisseria meningitidis.PLoS pathogens · 2021Article
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- Deconvolution of intergenic polymorphisms determining high expression of Factor H binding protein in meningococcus and their association with invasive disease.PLoS pathogens · 2021Article
- A Family Affair: Addressing the Challenges of Factor H and the Related Proteins.Frontiers in immunology · 2021Review
- Complement Genetic Variants and FH Desialylation inFrontiers in immunology · 2021Article
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Battlefronts of evolutionary conflict between bacteria and animal hosts.PLoS pathogens · 2020Article
- Complement Evasion Strategies of Human Pathogenic Bacteria.Indian journal of microbiology · 2020Review
- Human genetics of meningococcal infections.Human genetics · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Genome-wide association studies have found variation within the complement factor H gene family links to host susceptibility to meningococcal disease caused by infection with Neisseria meningitidis (Davila et al., 2010). Mechanistic insights have been challenging since variation within this locus is complex and biological roles of the factor H-related proteins, unlike factor H, are incompletely understood. N. meningitidis subverts immune responses by hijacking a host-immune regulator, complement factor H (CFH), to the bacterial surface (Schneider et al., 2006; Madico et al., 2007; Schneider et al., 2009). We demonstrate that complement factor-H related 3 (CFHR3) promotes immune activation by acting as an antagonist of CFH. Conserved sequences between CFH and CFHR3 mean that the bacterium cannot sufficiently distinguish between these two serum proteins to allow it to hijack the regulator alone. The level of protection from complement attack achieved by circulating N. meningitidis therefore depends on the relative levels of CFH and CFHR3 in serum. These data may explain the association between genetic variation in both CFH and CFHR3 and susceptibility to meningococcal disease.
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What OpenQuestion holds
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.