ArticleInfection and immunity2005
Demonstration of factor H-like protein 1 binding to Treponema denticola, a pathogen associated with periodontal disease in humans.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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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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
23 citing papers in PubMed, 45 citations in OpenAlex.
- Molecular Analysis ofPathogens (Basel, Switzerland) · 2024Article
- Subversion of the immune response of human pathogenic spirochetes.Journal of clinical laboratory analysis · 2022Review
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Tuning the Functionality by Splicing: Factor H and Its Alternative Splice Variant FHL-1 Share a Gene but Not All Functions.Frontiers in immunology · 2020Review
- Utilizing complement evasion strategies to design complement-based antibacterial immunotherapeutics: Lessons from the pathogenic Neisseriae.Immunobiology · 2016Review
- The Treponema denticola FhbB Protein Is a Dominant Early Antigen That Elicits FhbB Variant-Specific Antibodies That Block Factor H Binding and Cleavage by Dentilisin.Infection and immunity · 2016Article
- Analysis of the complement sensitivity of oral treponemes and the potential influence of FH binding, FH cleavage and dentilisin activity on the pathogenesis of periodontal disease.Molecular oral microbiology · 2014Article
- The Cross-Talk between Spirochetal Lipoproteins and Immunity.Frontiers in immunology · 2014Review
- A surface-exposed neuraminidase affects complement resistance and virulence of the oral spirochaete Treponema denticola.Molecular microbiology · 2013Article
- Sequence divergence in the Treponema denticola FhbB protein and its impact on factor H binding.Molecular oral microbiology · 2013Article
- Article
- Protease-dependent mechanisms of complement evasion by bacterial pathogens.Biological chemistry · 2012Review
- Structure of factor H-binding protein B (FhbB) of the periopathogen, Treponema denticola: insights into progression of periodontal disease.The Journal of biological chemistry · 2012Article
- Identification of the primary mechanism of complement evasion by the periodontal pathogen, Treponema denticola.Molecular oral microbiology · 2011Article
- Complement control protein factor H: the good, the bad, and the inadequate.Molecular immunology · 2010Review
- Immune evasion of leptospira species by acquisition of human complement regulator C4BP.Infection and immunity · 2009Article
- Identification of an antiparallel coiled-coil/loop domain required for ligand binding by the Borrelia hermsii FhbA protein: additional evidence for the role of FhbA in the host-pathogen interaction.Infection and immunity · 2008Article
- The opportunistic human pathogenic fungus Aspergillus fumigatus evades the host complement system.Infection and immunity · 2008Article
- Identification of the gene encoding the FhbB protein of Treponema denticola, a highly unique factor H-like protein 1 binding protein.Infection and immunity · 2007Article
- Binding of human complement regulators FHL-1 and factor H to CRASP-1 orthologs of Borrelia burgdorferi.Wiener klinische Wochenschrift · 2006Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treponema denticola is an important contributor to periodontal disease. In this study we investigated the ability of T. denticola to bind the complement regulatory proteins factor H and factor H-like protein 1 (FHL-1). The binding of these proteins has been demonstrated to facilitate evasion of the alternative complement cascade and/or to play a role in adherence and invasion. Here we demonstrate that T. denticola specifically binds FHL-1 via a 14-kDa, surface-exposed protein that we designated FhbB. Consistent with its FHL-1 binding specificity, FhbB binds only to factor H recombinant fragments spanning short consensus repeats (SCRs) 1 to 7 (H7 construct) and not to SCR constructs spanning SCRs 8 to 15 and 16 to 20. Binding of H7 to FhbB was inhibited by heparin. The specific involvement of SCR 7 in the interaction was demonstrated using an H7 mutant (H7AB) in which specific charged residues in SCR 7 were replaced by alanine. This construct lost FhbB binding ability. Analyses of the ability of FHL-1 bound to the surface of T. denticola to serve as a cofactor for factor I-mediated cleavage of C3b revealed that C3b is cleaved in an FHL-1/factor I-independent manner, perhaps by an unidentified protease. Based on the data presented here, we hypothesize that the primary function of FHL-1 binding by T. denticola might be to facilitate adherence to FHL-1 present on anchorage-dependent cells and in the extracellular matrix.
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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.