ArticlePLoS neglected tropical diseases2010
Human complement regulators C4b-binding protein and C1 esterase inhibitor interact with a novel outer surface protein of Borrelia recurrentis.
Article in PLoS neglected tropical diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Complement inhibition by a unique cluster of immunomodulatory outer surface proteins of Borrelia recurrentis.Nature communications · 2026Article
- BBK32 attenuates antibody-dependent complement-mediated killing of infectious Borreliella burgdorferi isolates.PLoS pathogens · 2025Article
- Whole-genome sequences of sixMicrobiology resource announcements · 2025Article
- Multifunctional interaction of CihC/FbpC orthologs of relapsing fever spirochetes with host-derived proteins involved in adhesion, fibrinolysis, and complement evasion.Frontiers in immunology · 2024Article
- Temporal patterns of gene expression in response to inoculation with a virulent Anaplasma phagocytophilum strain in sheep.Scientific reports · 2023Article
- Diverse Functions of C4b-Binding Protein in Health and Disease.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- "Conformational dynamics of C1r inhibitor proteins from Lyme disease and relapsing fever spirochetes".bioRxiv : the preprint server for biology · 2023Article
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- Mechanism of Borrelia immune evasion by FhbA-related proteins.PLoS pathogens · 2022Article
- Novel approaches for the serodiagnosis of louse-borne relapsing fever.Frontiers in cellular and infection microbiology · 2022Article
- Article
- Pathogenesis of Relapsing Fever.Current issues in molecular biology · 2021Review
- Interactions Between PathogenicFrontiers in cellular and infection microbiology · 2021Review
- Immune Evasion Strategies of Relapsing Fever Spirochetes.Frontiers in immunology · 2020Review
- Louse-borne relapsing fever (Borrelia recurrentis infection).Epidemiology and infection · 2019Review
- Genomic blueprint of a relapsing fever pathogen in 15th century Scandinavia.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Polymorphic factor H-binding activity of CspA protects Lyme borreliae from the host complement in feeding ticks to facilitate tick-to-host transmission.PLoS pathogens · 2018Article
- Virulence Associated Gene 8 ofFrontiers in immunology · 2018Article
- First insights in the variability of Borrelia recurrentis genomes.PLoS neglected tropical diseases · 2017Article
- Acquisition of C1 inhibitor by Bordetella pertussis virulence associated gene 8 results in C2 and C4 consumption away from the bacterial surface.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spirochete Borrelia recurrentis is the causal agent of louse-borne relapsing fever and is transmitted to humans by the infected body louse Pediculus humanus. We have recently demonstrated that the B. recurrentis surface receptor, HcpA, specifically binds factor H, the regulator of the alternative pathway of complement activation, thereby inhibiting complement mediated bacteriolysis. Here, we show that B. recurrentis spirochetes express another potential outer membrane lipoprotein, termed CihC, and acquire C4b-binding protein (C4bp) and human C1 esterase inhibitor (C1-Inh), the major inhibitors of the classical and lectin pathway of complement activation. A highly homologous receptor for C4bp was also found in the African tick-borne relapsing fever spirochete B. duttonii. Upon its binding to B. recurrentis or recombinant CihC, C4bp retains its functional potential, i.e. facilitating the factor I-mediated degradation of C4b. The additional finding that ectopic expression of CihC in serum sensitive B. burgdorferi significantly increased spirochetal resistance against human complement suggests this receptor to substantially contribute, together with other known strategies, to immune evasion of B. recurrentis.
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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.