ArticlePloS one2014
Induction of type I and type III interferons by Borrelia burgdorferi correlates with pathogenesis and requires linear plasmid 36.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Induction of indoleamine 2,3-dioxygenase by Borrelia burgdorferi in human immune cells correlates with pathogenic potential.Journal of leukocyte biology · 2015Trial
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Borrelia burgdorferi Outer Surface Protein C Is Not the Sole Determinant of Dissemination in Mammals.Infection and immunity · 2023Article
- Borrelia burgdorferi-mediated induction of miR146a-5p fine tunes the inflammatory response in human dermal fibroblasts.PloS one · 2023Article
- Recent Progress in Lyme Disease and Remaining Challenges.Frontiers in medicine · 2021Review
- Comprehensive Mapping of the Cell Response toFrontiers in microbiology · 2021Article
- The Lyme disease bacterium, Borrelia burgdorferi, stimulates an inflammatory response in human choroid plexus epithelial cells.PloS one · 2020Article
- Primordial origin and diversification of plasmids in Lyme disease agent bacteria.BMC genomics · 2018Article
- Genetic Control of Lyme Arthritis byJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Type III IFNs Are Commonly Induced by Bacteria-Sensing TLRs and Reinforce Epithelial Barriers during Infection.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Plasmid diversity and phylogenetic consistency in the Lyme disease agent Borrelia burgdorferi.BMC genomics · 2017Article
- Interferon Lambda: Modulating Immunity in Infectious Diseases.Frontiers in immunology · 2017Review
- Microbial pathogenesis and type III interferons.Cytokine & growth factor reviews · 2016Review
- Borrelia burgdorferi induces a type I interferon response during early stages of disseminated infection in mice.BMC microbiology · 2016Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The capacity for Borrelia burgdorferi to cause disseminated infection in humans or mice is associated with the genotype of the infecting strain. The cytokine profiles elicited by B. burgdorferi clinical isolates of different genotype (ribosomal spacer type) groups were assessed in a human PBMC co-incubation model. RST1 isolates, which are more frequently associated with disseminated Lyme disease in humans and mice, induced significantly higher levels of IFN-α and IFN-λ1/IL29 relative to RST3 isolates, which are less frequently associated with disseminated infection. No differences in the protein concentrations of IFN-γ, IL-1β, IL-6, IL-8, IL-10 or TNF-α were observed between isolates of differing genotype. The ability of B. burgdorferi to induce type I and type III IFNs was completely dependent on the presence of linear plasmid (lp) 36. An lp36-deficient B. burgdorferi mutant adhered to, and was internalized by, PBMCs and specific dendritic cell (DC) subsets less efficiently than its isogenic B31 parent strain. The association defect with mDC1s and pDCs could be restored by complementation of the mutant with the complete lp36. The RST1 clinical isolates studied were found to contain a 2.5-kB region, located in the distal one-third of lp36, which was not present in any of the RST3 isolates tested. This divergent region of lp36 may encode one or more factors required for optimal spirochetal recognition and the production of type I and type III IFNs by human DCs, thus suggesting a potential role for DCs in the pathogenesis of B. burgdorferi infection.
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Registered trials
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