ArticleInfection and immunity2004
Myeloid differentiation antigen 88 deficiency impairs pathogen clearance but does not alter inflammation in Borrelia burgdorferi-infected mice.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 147 citations in OpenAlex.
- Lipoprotein-dependent and -independent immune responses to spirochetal infection.Clinical and diagnostic laboratory immunology · 2005Trial
- Establishment of a laboratory mouse model to studyFrontiers in immunology · 2026Article
- Article
- Characterizing the impact of intracutaneous dissemination on host responses duringFrontiers in immunology · 2026Article
- Borrelia burgdorferi initiates early transcriptional re-programming in macrophages that supports long-term suppression of inflammation.PLoS pathogens · 2023Article
- Borrelia burgdorferi Infection-Induced Persistent IgM Secretion Controls Bacteremia, but Not Bacterial Dissemination or Tissue Burden.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Antigen-Specific CD4 T Cell and B Cell Responses to Borrelia burgdorferi.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- CD4 T cell responses in persistent Borrelia burgdorferi infection.Current opinion in immunology · 2022Review
- Pathogenesis of Borrelia burgdorferi and Babesia microti in TLR4-Competent and TLR4-dysfunctional C3H mice.Cellular microbiology · 2021Article
- Genetic Background Amplifies the Effect of Immunodeficiency in Antibiotic Efficacy Against Borrelia burgdorferi.The Journal of infectious diseases · 2021Article
- Macrophage mediated recognition and clearance of Borrelia burgdorferi elicits MyD88-dependent and -independent phagosomal signals that contribute to phagocytosis and inflammation.BMC immunology · 2021Article
- Live Imaging.Current issues in molecular biology · 2021Review
- Immune Response toCurrent issues in molecular biology · 2021Article
- A human secretome library screen reveals a role for Peptidoglycan Recognition Protein 1 in Lyme borreliosis.PLoS pathogens · 2020Article
- Rapid clearance of Borrelia burgdorferi from the blood circulation.Parasites & vectors · 2020Article
- Non-anticoagulant Heparin as a Pre-exposure Prophylaxis Prevents Lyme Disease Infection.ACS infectious diseases · 2020Article
- Regulation of macrophage activity by surface receptors contained within Borrelia burgdorferi-enriched phagosomal fractions.PLoS pathogens · 2019Article
- MyD88 Signaling in T Cells Is Critical for Effector CD4 T Cell Differentiation following a Transitional T Follicular Helper Cell Stage.Infection and immunity · 2018Article
- Genetic Control of Lyme Arthritis byJournal of immunology (Baltimore, Md. : 1950) · 2017Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The spirochete Borrelia burgdorferi causes acute inflammation in mice that resolves with the development of pathogen-specific adaptive immunity. B. burgdorferi lipoproteins activate innate immune cells via Toll-like receptor 2 (TLR2), but TLR2-deficient mice are not resistant to B. burgdorferi-induced disease, suggesting the involvement of other TLRs or non-TLR mechanisms in the induction of acute inflammation. For this study, we used mice that were deficient in the intracellular adapter molecule myeloid differentiation antigen 88 (MyD88), which is required for all TLR-induced inflammatory responses, to determine whether the interruption of this pathway would alter B. burgdorferi-induced disease. Infected MyD88(-/-) mice developed carditis and arthritis, similar to the disease in wild-type (WT) mice analyzed at its peak (days 14 and 28) and during regression (day 45). MyD88(-/-) macrophages produced tumor necrosis factor alpha only when spirochetes were opsonized, suggesting a role for B. burgdorferi-specific antibody in disease expression. MyD88(-/-) mice produced stronger pathogen-specific Th2-dependent immunoglobulin G1 (IgG1) responses than did WT mice, and their IgM titers remained significantly elevated through 90 days of infection. Despite specific antibodies, the pathogen burden was 250-fold higher in MyD88(-/-) mice than in WT mice 45 days after infection; by 90 days of infection, the pathogen burden had diminished substantially in MyD88(-/-) mice, but it was still elevated compared to that in WT mice. The elevated pathogen burden may be explained in part by the finding that MyD88(-/-) peritoneal macrophages could ingest spirochetes but degraded them more slowly than WT macrophages. Our results show that MyD88-dependent signaling pathways are not required for B. burgdorferi-induced inflammation but are necessary for the efficient control of the pathogen burden by phagocytes.
Indexed as
Identifiers
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.