ArticleCellular microbiology2019
Blood treatment of Lyme borreliae demonstrates the mechanism of CspZ-mediated complement evasion to promote systemic infection in vertebrate hosts.
Article in Cellular microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Complement therapeutic factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- Selection and characterization of DNA aptamers targeting the surface Borrelia protein CspZ with high-throughput cross-over SELEX.Communications biology · 2025Article
- Mechanistic insights into the structure-based design of a CspZ-targeting Lyme disease vaccine.Nature communications · 2025Article
- CspZ variant-specific interaction with factor H incorporates a metal site to support Lyme borreliae complement evasion.The Journal of biological chemistry · 2025Article
- Unveiling the impact ofInfection and immunity · 2024Article
- Mechanistic insights into structure-based design of a Lyme disease subunit vaccine.bioRxiv : the preprint server for biology · 2024Article
- Complement therapeutic Factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections.bioRxiv : the preprint server for biology · 2024Article
- Production, purification, and quality assessment of borrelial proteins CspZ from Borrelia burgdorferi and FhbA from Borrelia hermsii.Applied microbiology and biotechnology · 2024Article
- Highly heterogenous humoral immune response in Lyme disease patients revealed by broad machine learning-assisted antibody binding profiling with random peptide arrays.Frontiers in immunology · 2024Article
- Impact ofFrontiers in immunology · 2024Article
- The In Vitro Antimicrobial Susceptibility ofPathogens (Basel, Switzerland) · 2023Review
- Structural evolution of an immune evasion determinant shapes pathogen host tropism.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Past, present, and future of Lyme disease vaccines: antigen engineering approaches and mechanistic insights.Expert review of vaccines · 2022Review
- Phylogenomic Diversity Elucidates Mechanistic Insights into Lyme Borreliae-Host Association.mSystems · 2022Article
- CspZ FH-Binding Sites as Epitopes Promote Antibody-Mediated Lyme Borreliae Clearance.Infection and immunity · 2022Article
- Subversion of the immune response of human pathogenic spirochetes.Journal of clinical laboratory analysis · 2022Review
- Lipoproteome screening of the Lyme disease agent identifies inhibitors of antibody-mediated complement killing.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The evolving story of Borrelia burgdorferi sensu lato transmission in Europe.Parasitology research · 2022Review
- Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common vector-borne disease in the United States and Europe. The spirochetes are transmitted from mammalian and avian reservoir hosts to humans via ticks. Following tick bites, spirochetes colonize the host skin and then disseminate haematogenously to various organs, a process that requires this pathogen to evade host complement, an innate immune defence system. CspZ, a spirochete surface protein, facilitates resistance to complement-mediated killing in vitro by binding to the complement regulator, factor H (FH). Low expression levels of CspZ in spirochetes cultivated in vitro or during initiation of infection in vivo have been a major hurdle in delineating the role of this protein in pathogenesis. Here, we show that treatment of B. burgdorferi with human blood induces CspZ production and enhances resistance to complement. By contrast, a cspZ-deficient mutant and a strain that expressed an FH-nonbinding CspZ variant were impaired in their ability to cause bacteraemia and colonize tissues of mice or quail; virulence of these mutants was however restored in complement C3-deficient mice. These novel findings suggest that FH binding to CspZ facilitates B. burgdorferi complement evasion in vivo and promotes systemic infection in vertebrate hosts.
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