ArticleInfection and immunity2014
MyD88- and TRIF-independent induction of type I interferon drives naive B cell accumulation but not loss of lymph node architecture in Lyme disease.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 42 citations in OpenAlex.
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Borrelia burgdorferi sensu lato Employs Several Escape Mechanisms to Bypass the Human Defense System.European journal of immunology · 2026Review
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Role of dual specificity phosphatase 1 in influencing inflammatory pathways in macrophages modulated byFrontiers in immunology · 2026Article
- Extrafollicular and Other Non-Germinal Center B Cell Responses: An Evolutionary Perspective.Immunological reviews · 2025Review
- Role of Dual Specificity Phosphatase 1 (DUSP1) in influencing inflammatory pathways in macrophages modulated bybioRxiv : the preprint server for biology · 2025Article
- Antibody-mediated immunological memory correlates with long-term Lyme veterinary vaccine protection in mice.Vaccine · 2024Article
- 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
- Immune evasion strategies of major tick-transmitted bacterial pathogens.Trends in microbiology · 2023Review
- Comparative transcriptome analysis ofFrontiers in cellular and infection microbiology · 2023Article
- Recent Advances in the Immunologic Method Applied to Tick-Borne Diseases in Brazil.Pathogens (Basel, Switzerland) · 2022Review
- CD4 T cell responses in persistent Borrelia burgdorferi infection.Current opinion in immunology · 2022Review
- The Shaping of a B Cell Pool Maximally Responsive to Infections.Annual review of immunology · 2021Article
- The Brilliance ofPathogens (Basel, Switzerland) · 2021Review
- A murine model of Lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system.PLoS pathogens · 2021Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Germinal Center and Extrafollicular B Cell Responses in Vaccination, Immunity, and Autoimmunity.Immunity · 2020Review
- Comparison of spleen transcriptomes of two wild rodent species reveals differences in the immune response againstEcology and evolution · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88- and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity.
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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.