ArticleClinical & developmental immunology2012
Contribution of the infection-associated complement regulator-acquiring surface protein 4 (ErpC) to complement resistance of Borrelia burgdorferi.
Article in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
The trial behind it
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
27 citing papers in PubMed, 38 citations in OpenAlex.
- Navigating infection by pathogenic spirochetes: The host-bacteria interface at the atomic level.Protein science : a publication of the Protein Society · 2025Review
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- Comparative genomics analysis of three conserved plasmid families in the Western Hemisphere soft tick-borne relapsing fever borreliae provides insight into variation in genome structure and antigenic variation systems.Microbiology spectrum · 2023Article
- Comparative genomics analysis of three conserved plasmid families in the Western Hemisphere soft tick-borne relapsing fever borreliae provides insight into variation in genome structure and antigenic variation systems.bioRxiv : the preprint server for biology · 2023Article
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- New Insights Into CRASP-Mediated Complement Evasion in the Lyme Disease Enzootic Cycle.Frontiers in cellular and infection microbiology · 2020Review
- Outer surface protein polymorphisms linked to host-spirochete association in Lyme borreliae.Molecular microbiology · 2019Review
- Elucidating the Immune Evasion Mechanisms ofFrontiers in immunology · 2019Article
- A bite so sweet: the glycobiology interface of tick-host-pathogen interactions.Parasites & vectors · 2018Review
- 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
- Further Insights Into the Interaction of Human and Animal Complement Regulator Factor H With Viable Lyme Disease Spirochetes.Frontiers in veterinary science · 2018Article
- Borrelia burgdorferi outer surface protein C (OspC) binds complement component C4b and confers bloodstream survival.Cellular microbiology · 2017Article
- Immune evasion of Borrelia miyamotoi: CbiA, a novel outer surface protein exhibiting complement binding and inactivating properties.Scientific reports · 2017Article
- There Is a Method to the Madness: Strategies to Study Host Complement Evasion by Lyme Disease and Relapsing Fever Spirochetes.Frontiers in microbiology · 2017Review
- Crystal structure of a tripartite complex between C3dg, C-terminal domains of factor H and OspE of Borrelia burgdorferi.PloS one · 2017Article
- Travelling between Two Worlds: Complement as a Gatekeeper for an Expanded Host Range of Lyme Disease Spirochetes.Veterinary sciences · 2016Review
- Multifunctional and Redundant Roles ofFrontiers in immunology · 2016Review
- Hide and Seek: How Lyme Disease Spirochetes Overcome Complement Attack.Frontiers in immunology · 2016Review
- A short-term Borrelia burgdorferi infection model identifies tissue tropisms and bloodstream survival conferred by adhesion proteins.Infection and immunity · 2015Article
- Factor H-related protein 5 interacts with pentraxin 3 and the extracellular matrix and modulates complement activation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Borrelia burgdorferi evades complement-mediated killing by interacting with complement regulators through distinct complement regulator-acquiring surface proteins (CRASPs). Here, we extend our analyses to the contribution of CRASP-4 in mediating complement resistance of B. burgdorferi and its interaction with human complement regulators. CRASP-4 (also known as ErpC) was immobilized onto magnetic beads and used to capture proteins from human serum. Following Western blotting, factor H (CFH), CFH-related protein 1 (CFHR1), CFHR2, and CFHR5 were identified as ligands of CRASP-4. To analyze the impact of native CRASP-4 on mediating survival of serum-sensitive cells in human serum, a B. garinii strain was generated that ectopically expresses CRASP-4. CRASP-4-producing bacteria bound CFHR1, CFHR2, and CFHR5 but not CFH. In addition, transformed spirochetes deposited significant amounts of lethal complement components on their surface and were susceptible to human serum, thus indicating that CRASP-4 plays a subordinate role in complement resistance of B. burgdorferi.
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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.