ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Endothelial cells and fibroblasts amplify the arthritogenic type I IFN response in murine Lyme disease and are major sources of chemokines in Borrelia burgdorferi-infected joint tissue.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 44 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
- Spatial Transcriptomic Profiling Reveals Microenvironment-Dependent Immune Signatures in a Lyme Arthritis model.bioRxiv : the preprint server for biology · 2026Article
- Infection-Triggered Immune Dysregulation and Immunopathology in Lyme Disease: Mechanisms and Clinical Implications.Journal of clinical medicine · 2026Review
- Strain-specific immune response patterns toInfection and immunity · 2026Article
- Making the best of a sticky situation: Infection-mediated endothelial activation promotes new interactions with adhesins of the host-adapted Lyme disease spirochete.bioRxiv : the preprint server for biology · 2026Article
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- HLA-DR-Expressing Fibroblast-Like Synoviocytes Are Inducible Antigen Presenting Cells That Present Autoantigens in Lyme Arthritis.ACR open rheumatology · 2024Article
- Identification of Major Histocompatibility Complex Class II Epitopes From Lyme Autoantigen Apolipoprotein B-100 and Borrelia burgdorferi Mcp4 in Murine Lyme Arthritis.The Journal of infectious diseases · 2024Article
- Comparative reservoir competence ofApplied and environmental microbiology · 2024Article
- Development of Organoids to Study Infectious Host Interactions.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Borrelia burgdorferi initiates early transcriptional re-programming in macrophages that supports long-term suppression of inflammation.PLoS pathogens · 2023Article
- Human leukocyte antigen HLA-DR-expressing fibroblast-like synoviocytes are inducible antigen presenting cells that present autoantigens in Lyme arthritis.bioRxiv : the preprint server for biology · 2023Article
- Single-cell RNA sequencing of murine ankle joints over time reveals distinct transcriptional changes followingiScience · 2023Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Endogenous Linear Plasmids lp28-4 and lp25 Are Required for Infectivity and Restriction Protection in the Lyme Disease Spirochete Borrelia mayonii.Infection and immunity · 2023Article
- Review
- 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 Cdkn2a gene product p19 alternative reading frame (p19ARF) is a critical regulator of IFNβ-mediated Lyme arthritis.PLoS pathogens · 2022Article
- Lyme arthritis: linking infection, inflammation and autoimmunity.Nature reviews. Rheumatology · 2021Review
- Host transcriptome response to Borrelia burgdorferi sensu lato.Ticks and tick-borne diseases · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Localized elevation in type I IFN has been uniquely linked to the severe Lyme arthritis that develops in C3H mice infected with the spirochete Borrelia burgdorferi. In this study, the dynamic interactions that result in generation of these responses were further examined in C3H mice carrying the type I IFN receptor gene ablation, which effectively blocks all autocrine/paracrine signaling crucial to induction of downstream effectors. Reciprocal radiation chimeras between C3H and IFNAR1⁻/⁻ mice implicated both radiation-sensitive and radiation-resistant cells of the joint tissue in the proarthritic induction of type I IFN. Ex vivo analysis of cells from the naive joint revealed CD45⁺ cells residing in the tissue to be uniquely capable of initiating the type I IFN response to B. burgdorferi. Type I IFN responses were analyzed in real time by lineage sorting of cells from infected joint tissue. This demonstrated that myeloid cells, endothelial cells, and fibroblasts were responsible for propagating the robust IFN response, which peaked at day 7 postinfection and rapidly resolved. Endothelial cells and fibroblasts were the dominant sources of IFN signature transcripts in the joint tissue. Fibroblasts were also the major early source of chemokines associated with polymorphonuclear leukocyte and monocyte/macrophage infiltration, thus providing a focal point for arthritis development. These findings suggest joint-localized interactions among related and unrelated stromal, endothelial, and myeloid cell lineages that may be broadly applicable to understanding the pathogeneses of diseases associated with type I IFN signature, including systemic lupus erythematosus and some rheumatoid arthritides.
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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.