ArticleThe Journal of biological chemistry2008
Deciphering the ligand-binding sites in the Borrelia burgdorferi complement regulator-acquiring surface protein 2 required for interactions with the human immune regulators factor H and factor H-like protein 1.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- Natural genetic variation impacts complement inhibitory activity of PFam54 orthologs of Asian Borrelia bavariensis.Scientific reports · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- 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
- Mechanistic insights into structure-based design of a Lyme disease subunit vaccine.bioRxiv : the preprint server for biology · 2024Article
- Article
- 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
- Utilizing Two Borrelia bavariensis Isolates Naturally Lacking the PFam54 Gene Array To Elucidate the Roles of PFam54-Encoded Proteins.Applied and environmental microbiology · 2022Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- The Factor H-Binding Site of CspZ as a Protective Target against Multistrain, Tick-Transmitted Lyme Disease.Infection and immunity · 2020Article
- New Insights Into CRASP-Mediated Complement Evasion in the Lyme Disease Enzootic Cycle.Frontiers in cellular and infection microbiology · 2020Review
- Downregulated expression of CFHL1 is associated with unfavorable prognosis in postoperative patients with hepatocellular carcinoma.Experimental and therapeutic medicine · 2019Article
- Outer surface protein polymorphisms linked to host-spirochete association in Lyme borreliae.Molecular microbiology · 2019Review
- Blood treatment of Lyme borreliae demonstrates the mechanism of CspZ-mediated complement evasion to promote systemic infection in vertebrate hosts.Cellular microbiology · 2019Article
- Elucidating the Immune Evasion Mechanisms ofFrontiers in immunology · 2019Article
- A bite so sweet: the glycobiology interface of tick-host-pathogen interactions.Parasites & vectors · 2018Review
- Eliminating Factor H-Binding Activity ofFrontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Borrelia burgdorferi, the etiologic agent of Lyme disease, employs sophisticated means to evade killing by its mammalian hosts. One important immune escape mechanism is the inhibition of complement activation mediated by interactions of the host-derived immune regulators factor H (CFH) and factor H-like protein 1 (CFHL1) with borrelial complement regulator-acquiring surface proteins (BbCRASPs). BbCRASP-2 is a distinctive CFH- and CFHL1-binding protein that is produced by serum-resistant B. burgdorferi strains. Here we show that binding of CFH by BbCRASP-2 is due to electrostatic as well as hydrophobic forces. In addition, 14 individual amino acid residues of BbCRASP-2 were identified as being involved in CFH and CFHL1 binding. Alanine substitutions of most of those residues significantly inhibited binding of CFH and/or CFHL1 by recombinant BbCRASP-2 proteins. To conclusively define the effects of BbCRASP-2 residue substitutions on serum sensitivity in the bacterial context, a serum-sensitive Borrelia garinii strain was transformed with plasmids that directed production of either wild-type or mutated BbCRASP-2 proteins. Critical amino acid residues within BbCRASP-2 were identified, with bacteria producing distinct mutant proteins being unable to bind either CFH or CFHL1, showing high levels of complement components C3, C6, and C5b-9 deposited on their surfaces and being highly sensitive to killing by normal serum. Collectively, we mapped a structurally sensitive CFH/CFHL1 binding site within borrelial BbCRASP-2 and identified single amino acid residues potentially involved in the interaction with both complement regulators.
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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.