ArticleArthritis research & therapy2017
Priming in response to pro-inflammatory cytokines is a feature of adult synovial but not dermal fibroblasts.
Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
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- The distinct transcriptomic signature of the resolution phase fibroblast-like synoviocytes supports endothelial cell dysfunction.Communications biology · 2025Article
- Pro-Inflammatory Properties of Salivary Gland-Derived Fibroblasts-Implications in Sjögren's Disease.Cells · 2025Article
- Antioxidant Therapies as Emerging Adjuncts in Rheumatoid Arthritis: Targeting Oxidative Stress to Enhance Treatment Outcomes.International journal of molecular sciences · 2025Review
- Methotrexate promotes the release of granulocyte-macrophage colony-stimulating factor from rheumatoid arthritis fibroblast-like synoviocytes via autocrine interleukin-1 signaling.Arthritis research & therapy · 2024Article
- Joint-specific memory, resident memory T cells and the rolling window of opportunity in arthritis.Nature reviews. Rheumatology · 2024Review
- Epigenetic regulation of innate immune dynamics during inflammation.Journal of leukocyte biology · 2024Review
- Synovial fibroblasts from children with oligoarticular juvenile idiopathic arthritis induce migration and prolong viability of neutrophils.Frontiers in pediatrics · 2024Article
- Article
- Fibroblast heterogeneity: Keystone of tissue homeostasis and pathology in inflammation and ageing.Frontiers in immunology · 2023Review
- Molecular and morphological alterations in uninjured skin of streptozotocin-induced diabetic mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Review
- Human Lung Fibroblasts Exhibit Induced Inflammation MemoryFrontiers in immunology · 2022Article
- Fibroblasts as immune regulators in infection, inflammation and cancer.Nature reviews. Immunology · 2021Review
- Review
- Targeting of Janus Kinases Limits Pro-Inflammatory but Also Immunosuppressive Circuits in the Crosstalk between Synovial Fibroblasts and Lymphocytes.Biomedicines · 2021Article
- Dietary Derived Propionate Regulates Pathogenic Fibroblast Function and Ameliorates Experimental Arthritis and Inflammatory Tissue Priming.Nutrients · 2021Article
- Location, location, location: how the tissue microenvironment affects inflammation in RA.Nature reviews. Rheumatology · 2021Review
- Increase of aerobic glycolysis mediated by activated T helper cells drives synovial fibroblasts towards an inflammatory phenotype: new targets for therapy?Arthritis research & therapy · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIt has been hypothesized that chronic inflammatory diseases such as rheumatoid arthritis (RA) may be caused by a failure of negative feedback mechanisms. This study sought to examine negative feedback mechanisms in fibroblast-like synoviocytes (FLS), one of the most abundant cell types in the joint. We hypothesized that prior exposure of healthy FLS to an inflammatory stimulus would attenuate their responses to a second inflammatory stimulus, in the same way that negative feedback mechanisms desensitize macrophages to repeated stimulation by lipopolysaccharide. We further hypothesized that such negative feedback mechanisms would be defective in FLS derived from the joints in RA.
methodsSynovial fibroblasts and dermal fibroblasts from non-inflamed joints and joints affected by RA and a fibroblast cell line from neonatal foreskin were stimulated twice with tumour necrosis factor (TNF) α or interleukin (IL)-1α, with a 24-h rest period between the two 24-h stimulations. Differences between response to the first and second dose of cytokine were examined by assessing secretion of inflammatory factors and intracellular signalling activity.
resultsFLS from both non-inflamed joints and joints affected by RA mounted an augmented response to re-stimulation. This response was site-specific, as primary dermal fibroblasts did not alter their response between doses. The fibroblast priming was also gene-specific and transient. Assessment of signalling events and nuclear localization showed prolonged activation of nuclear factor (NF)-κB during the second stimulation.
conclusionThis study aimed to examine mechanisms of negative regulation of inflammatory responses in FLS. Instead, we found a pro-inflammatory stromal memory in FLS obtained from both non-inflamed joints and joints affected by RA. This suggests the joint is an area at high risk of chronic inflammation, and may provide a piece in the puzzle of how chronic inflammation is established in RA.
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Registered trials
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