ArticlePloS one2010
Complement factor H-related proteins CFHR2 and CFHR5 represent novel ligands for the infection-associated CRASP proteins of Borrelia burgdorferi.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
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- The plasmid-encoded members of paralogous gene family 52 are dispensable to the enzootic cycle ofInfection and immunity · 2024Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- Immune evasion strategies of major tick-transmitted bacterial pathogens.Trends in microbiology · 2023Review
- PathogenicInfection and immunity · 2022Article
- 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
- Potential Regulatory Role in Mammalian Host Adaptation for a Small Intergenic Region of Lp17 in the Lyme Disease Spirochete.Frontiers in cellular and infection microbiology · 2022Article
- Vitronectin binding protein, BOM1093, confers serum resistance on Borrelia miyamotoi.Scientific reports · 2021Article
- The Brilliance ofPathogens (Basel, Switzerland) · 2021Review
- Analysis of complement deposition and processing on Chlamydia trachomatis.Medical microbiology and immunology · 2021Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- Screening and identification of serum biomarkers of osteoarticular tuberculosis based on mass spectrometry.Journal of clinical laboratory analysis · 2020Article
- New Insights Into CRASP-Mediated Complement Evasion in the Lyme Disease Enzootic Cycle.Frontiers in cellular and infection microbiology · 2020Review
- Serum FHR1 binding to necrotic-type cells activates monocytic inflammasome and marks necrotic sites in vasculopathies.Nature communications · 2019Article
- 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
- Elucidating the Immune Evasion Mechanisms ofFrontiers in immunology · 2019Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundOne virulence property of Borrelia burgdorferi is its resistance to innate immunity, in particular to complement-mediated killing. Serum-resistant B. burgdorferi express up to five distinct complement regulator-acquiring surface proteins (CRASP) which interact with complement regulator factor H (CFH) and factor H-like protein 1 (FHL1) or factor H-related protein 1 (CFHR1). In the present study we elucidate the role of the infection-associated CRASP-3 and CRASP-5 protein to serve as ligands for additional complement regulatory proteins as well as for complement resistance of B. burgdorferi. METHODOLOGY/PRINCIPAL
findingsTo elucidate whether CRASP-5 and CRASP-3 interact with various human proteins, both borrelial proteins were immobilized on magnetic beads. Following incubation with human serum, bound proteins were eluted and separated by Glycine-SDS-PAGE. In addition to CFH and CFHR1, complement regulators CFHR2 and CFHR5 were identified as novel ligands for both borrelial proteins by employing MALDI-TOF. To further assess the contributions of CRASP-3 and CRASP-5 to complement resistance, a serum-sensitive B. garinii strain G1 which lacks all CFH-binding proteins was used as a valuable model for functional analyses. Both CRASPs expressed on the B. garinii outer surface bound CFH as well as CFHR1 and CFHR2 in ELISA. In contrast, live B. garinii bound CFHR1, CFHR2, and CFHR5 and only miniscute amounts of CFH as demonstrated by serum adsorption assays and FACS analyses. Further functional analysis revealed that upon NHS incubation, CRASP-3 or CRASP-5 expressing borreliae were killed by complement. CONCLUSIONS/SIGNIFICANCE: In the absence of CFH and the presence of CFHR1, CFHR2 and CFHR5, assembly and integration of the membrane attack complex was not efficiently inhibited indicating that CFH in co-operation with CFHR1, CFHR2 and CFHR5 supports complement evasion of B. burgdorferi.
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