ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Localized production of IL-10 suppresses early inflammatory cell infiltration and subsequent development of IFN-γ-mediated Lyme arthritis.
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 40 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
40 citing papers in PubMed, 57 citations in OpenAlex.
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Characterizing the impact of intracutaneous dissemination on host responses duringFrontiers in immunology · 2026Article
- Article
- Alpha-galactosylceramide pre-treatment attenuates clinical symptoms of LPS-induced acute neuroinflammation by converting pathogenic iNKT cells to anti-inflammatory iNKT10 cells in the brain.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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
- 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
- Effects of Regulatory T Cell Depletion in BALB/c Mice Infected with Low Doses ofPathogens (Basel, Switzerland) · 2023Article
- Comparative transcriptome analysis ofFrontiers in cellular and infection microbiology · 2023Article
- Polyethylene Glycol-grafted poly alpha-lipoic acid-dexamethasone nanoparticles for osteoarthritis.Frontiers in drug delivery · 2023Article
- The PD-1/PD-L1 pathway is induced during Borrelia burgdorferi infection and inhibits T cell joint infiltration without compromising bacterial clearance.PLoS pathogens · 2022Article
- CD4 T cell responses in persistent Borrelia burgdorferi infection.Current opinion in immunology · 2022Review
- 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
- Molecular Mechanisms ofBiology · 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
- Robust interferon signature and suppressed tissue repair gene expression in synovial tissue from patients with postinfectious, Borrelia burgdorferi-induced Lyme arthritis.Cellular microbiology · 2019Article
- Interferon-gamma production in Lyme arthritis synovial tissue promotes differentiation of fibroblast-like synoviocytes into immune effector cells.Cellular microbiology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
IL-10 is a nonredundant inflammatory modulator that suppresses arthritis development in Borrelia burgdorferi-infected mice. Infected C57BL/6 (B6) IL-10(-/-) mice were previously found to have a prolonged IFN-inducible response in joint tissue. Infection of B6 IL-10 reporter mice identified macrophages and CD4(+) T cells as the primary sources of IL-10 in the infected joint tissue, suggesting that early local production of IL-10 dampened the proarthritic IFN response. Treatment of B6 IL-10(-/-) mice with anti-IFN-γ reduced the increase in arthritis severity and suppressed IFN-inducible transcripts to wild-type levels, thereby linking dysregulation of IFN-γ to disease in the B6 IL-10(-/-) mouse. Arthritis in B6 IL-10(-/-) mice was associated with elevated numbers of NK cell, NKT cell, α/β T cell, and macrophage infiltration of the infected joint. FACS lineage sorting revealed NK cells and CD4(+) T cells as sources of IFN-γ in the joint tissue of B6 IL-10(-/-) mice. These findings suggest the presence of a positive-feedback loop in the joint tissue of infected B6 IL-10(-/-) mice, in which production of inflammatory chemokines, infiltration of IFN-γ-producing cells, and additional production of inflammatory cytokines result in arthritis. This mechanism of arthritis is in contrast to that seen in C3H/He mice, in which arthritis development is linked to transient production of type I IFN and develops independently of IFN-γ. Due to the sustained IFN response driven by NK cells and T cells, we propose the B6 IL-10(-/-) mouse as a potential model to study the persistent arthritis observed in some human Lyme disease patients.
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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.