ArticleCellular microbiology2019
Interferon-gamma production in Lyme arthritis synovial tissue promotes differentiation of fibroblast-like synoviocytes into immune effector cells.
Article in Cellular microbiology, 2019. 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, 50 citations in OpenAlex.
- Antiphospholipid antibodies in acute and post-treatment Lyme disease.Infection and immunity · 2026Article
- Borrelia burgdorferi sensu lato Employs Several Escape Mechanisms to Bypass the Human Defense System.European journal of immunology · 2026Review
- Single-cell immunophenotyping identifies CD8+GZMK+IFNG+ T cells as a key immune population in cutaneous Lyme disease.JCI insight · 2026Article
- Characterizing the impact of intracutaneous dissemination on host responses duringFrontiers in immunology · 2026Article
- Aspects of the Immunopathogenesis of Lyme Arthritis.Microorganisms · 2025Review
- Article
- Synovial fluid alpha-defensins in Lyme arthritis-a useful marker.Folia microbiologica · 2024Article
- Bridging the gap: Insights in the immunopathology of Lyme borreliosis.European journal of immunology · 2024Review
- The immune landscape of the inflamed joint defined by spectral flow cytometry.Clinical and experimental immunology · 2024Article
- HLA-DR-Expressing Fibroblast-Like Synoviocytes Are Inducible Antigen Presenting Cells That Present Autoantigens in Lyme Arthritis.ACR open rheumatology · 2024Article
- Variants in the Late Cornified Envelope Gene Locus Are Associated With Elevated T-helper 17 Responses in Patients With Postinfectious Lyme Arthritis.The Journal of infectious diseases · 2024Article
- Lyme Arthritis: A 50-Year Journey.The Journal of infectious diseases · 2024Article
- Fibroblast: A Novel Target for Autoimmune and Inflammatory Skin Diseases Therapeutics.Clinical reviews in allergy & immunology · 2024Review
- 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
- Autoimmunity to synovial extracellular matrix proteins in patients with postinfectious Lyme arthritis.The Journal of clinical investigation · 2023Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Cell-Mediated Cytotoxicity in Lyme Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- The regulation of self-tolerance and the role of inflammasome molecules.Frontiers in immunology · 2023Review
- Lyme disease and the pursuit of a clinical cure.Frontiers in medicine · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Lyme arthritis (LA), a late disease manifestation of Borrelia burgdorferi infection, usually resolves with antibiotic therapy. However, some patients develop proliferative synovitis lasting months to several years after spirochetal killing, called postinfectious LA. In this study, we phenotyped haematopoietic and stromal cell populations in the synovial lesion ex vivo and used these findings to generate an in vitro model of LA using patient-derived fibroblast-like synoviocytes (FLS). Ex vivo analysis of synovial tissue revealed high abundance of IFNγ-producing T cells and NK cells. Similar to marked IFNγ responses in tissue, postinfectious LA synovial fluid also had high levels of IFNγ. HLA-DR-positive FLS were present throughout the synovial lesion, particularly in areas of inflammation. FLS stimulated in vitro with B. burgdorferi, which were similar to conditions during infection, expressed 68 genes associated primarily with innate immune activation and neutrophil recruitment. In contrast, FLS stimulated with IFNγ, which were similar to conditions in the postinfectious phase, expressed >2,000 genes associated with pathogen sensing, inflammation, and MHC Class II antigen presentation, similar to the expression profile in postinfectious synovial tissue. Furthermore, costimulation of FLS with B. burgdorferi and IFNγ induced greater expression of IL-6 and other innate immune response proteins and genes than with IFNγ stimulation alone. These results suggest that B. burgdorferi infection, in combination with IFNγ, initiates the differentiation of FLS into a highly inflammatory phenotype. We hypothesise that overexpression of IFNγ by lymphocytes within synovia perpetuates these responses in the postinfectious period, causing proliferative synovitis and stalling appropriate repair of damaged tissue.
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