ArticlePloS one2013
Borrelia burgdorferi elicited-IL-10 suppresses the production of inflammatory mediators, phagocytosis, and expression of co-stimulatory receptors by murine macrophages and/or dendritic cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 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.
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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
37 citing papers in PubMed, 54 citations in OpenAlex.
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- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Interlaboratory Concordance of a Multiplex ELISA for Lyme and Lyme-like Illness Using Australian Samples and Commercial Reference Panels: A Proof-of-Concept Study.Pathogens (Basel, Switzerland) · 2025Article
- BBK32 attenuates antibody-dependent complement-mediated killing of infectious Borreliella burgdorferi isolates.PLoS pathogens · 2025Article
- Secreted Metabolites fromMicroorganisms · 2024Article
- Genome-wide analyses in Lyme borreliosis: identification of a genetic variant associated with disease susceptibility and its immunological implications.BMC infectious diseases · 2024Article
- A chemosensory-like histidine kinase is dispensable for chemotaxis in vitro but regulates the virulence of Borrelia burgdorferi through modulating the stability of RpoS.PLoS pathogens · 2023Article
- Screening of Optimal CpG-Oligodeoxynucleotide for Anti-Inflammatory Responses in the Avian Macrophage Cell Line HD11.The journal of poultry science · 2023Article
- Cellular and transcriptome signatures unveiled by single-cell RNA-Seq followingFrontiers in immunology · 2023Article
- Interference with LTβR signaling by tick saliva facilitates transmission of Lyme disease spirochetes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Impact of Severe COVID-19 on Plasma Antioxidants.Molecules (Basel, Switzerland) · 2022Article
- Subversion of the immune response of human pathogenic spirochetes.Journal of clinical laboratory analysis · 2022Review
- Redox Imbalance and Its Metabolic Consequences in Tick-Borne Diseases.Frontiers in cellular and infection microbiology · 2022Review
- Systemic immune responses in patients with early localized or early disseminated Borrelia afzelii lyme borreliosis.Immunity, inflammation and disease · 2021Article
- Assessing the Need for Multiplex and Multifunctional Tick-Borne Disease Test in Routine Clinical Laboratory Samples from Lyme Disease and Febrile Patients with a History of a Tick Bite.Tropical medicine and infectious disease · 2021Article
- The Brilliance ofPathogens (Basel, Switzerland) · 2021Review
- Immune Response toCurrent issues in molecular biology · 2021Article
- Innate Immune Memory to RepeatedJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Regulatory T Cells Contribute to Resistance against Lyme Arthritis.Infection and immunity · 2020Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Borrelia burgdorferi (Bb) is a tick-borne spirochete that is the causative agent for Lyme disease. Our previous studies indicate that virulent Bb can potently enhance IL-10 production by macrophages (MØs) and that blocking IL-10 production significantly enhances bacterial clearance. We hypothesize that skin-associated APC types, such as MØs and dendritic cells (DCs) are potent producers of IL-10 in response to Bb, which may act in autocrine fashion to suppress APC responses critical for efficient Bb clearance. Our goal is to delineate which APC immune functions are dysregulated by Bb-elicited IL-10 using a murine model of Lyme disease. Our in vitro studies indicated that both APCs rapidly produce IL-10 upon exposure to Bb, that these levels inversely correlate with the production of many Lyme-relevant proinflammatory cytokines and chemokines, and that APCs derived from IL-10(-/-) mice produced greater amounts of these proinflammatory mediators than wild-type APCs. Phagocytosis assays determined that Bb-elicited IL-10 levels can diminish Bb uptake and trafficking by MØs, suppresses ROS production, but does not affect NO production; Bb-elicited IL-10 had little effect on phagocytosis, ROS, and NO production by DCs. In general, Bb exposure caused little-to-no upregulation of several critical surface co-stimulatory markers by MØs and DCs, however eliminating Bb-elicited IL-10 allowed a significant upregulation in many of these co-stimulatory receptors. These data indicate that IL-10 elicited from Bb-stimulated MØs and DCs results in decreased production of proinflammatory mediators and co-stimulatory molecules, and suppress phagocytosis-associated events that are important for mediating both innate and adaptive immune responses by APCs.
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What OpenQuestion holds
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.