ArticleRheumatology international2005
The production of CXCR3-agonistic chemokines by synovial fibroblasts from patients with rheumatoid arthritis.
Article in Rheumatology international, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 71 citations in OpenAlex.
- The Developmental and Functional Implications of Age-Associated B Cells (ABCs) Across Tissue Microenvironments.Immunological reviews · 2026Review
- Targeting fibroblasts in immune mediated inflammatory diseases: a cellular basis for cure?Rheumatology (Oxford, England) · 2026Review
- Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.Clinical reviews in allergy & immunology · 2025Review
- Redefinition of Synovial Fibroblasts in Rheumatoid Arthritis.Aging and disease · 2024Review
- Regulation of cytokine and chemokine expression by histone lysine methyltransferase MLL1 in rheumatoid arthritis synovial fibroblasts.Scientific reports · 2024Article
- Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity.Cell communication and signaling : CCS · 2024Article
- Autoreactive B cells in rheumatoid arthritis include mainly activated CXCR3+ memory B cells and plasmablasts.JCI insight · 2023Article
- Efficacy of COVID-19 mRNA vaccination in patients with autoimmune disorders: humoral and cellular immune response.BMC medicine · 2023Article
- A review of the pleiotropic actions of the IFN-inducible CXC chemokine receptor 3 ligands in the synovial microenvironment.Cellular and molecular life sciences : CMLS · 2023Review
- Fibroblast heterogeneity: Keystone of tissue homeostasis and pathology in inflammation and ageing.Frontiers in immunology · 2023Review
- The synovial fluid fibroblast-like synoviocyte: A long-neglected piece in the puzzle of rheumatoid arthritis pathogenesis.Frontiers in immunology · 2022Review
- Identification of hub genes and therapeutic drugs in rheumatoid arthritis patients.Clinical rheumatology · 2021Article
- Destructive Roles of Fibroblast-like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis.Inflammation · 2021Review
- The pathogenic importance of CCL21 and CCR7 in rheumatoid arthritis.Cytokine & growth factor reviews · 2020Review
- FOXO3 is involved in the tumor necrosis factor-driven inflammatory response in fibroblast-like synoviocytes.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Regulation of Immune Responses and Chronic Inflammation by Fibroblast-Like Synoviocytes.Frontiers in immunology · 2019Review
- The Rheumatoid Arthritis Risk Gene AIRE Is Induced by Cytokines in Fibroblast-Like Synoviocytes and Augments the Pro-inflammatory Response.Frontiers in immunology · 2019Article
- mTOR Senses Environmental Cues to Shape the Fibroblast-like Synoviocyte Response to Inflammation.Cell reports · 2018Article
- Blood chemokine profile in untreated early rheumatoid arthritis: CXCL10 as a disease activity marker.Arthritis research & therapy · 2017Article
- Progranulin inhibits expression and release of chemokines CXCL9 and CXCL10 in a TNFR1 dependent manner.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflamed synovial tissue of rheumatoid arthritis (RA) is characterized by an infiltration with Th1 cells that predominantly express the chemokine receptors CXCR3 and CCR5. In this study, we investigated the production of the CXCR3-agonistic chemokines CXCL9, CXCL10, and CXCL11 by synovial tissue cells and synovial fibroblast-cell lines (fourth or fifth passage) from RA patients. Concentrations of all CXCR3 ligands in synovial fluids were markedly higher in RA patients than in osteoarthritis (OA) patients. Synovial tissue cells from RA patients more strongly expressed mRNAs for CXCR3 ligands and spontaneously secreted larger amounts of these chemokine proteins than the cells from OA patients. The mRNA expression of all CXCR3 ligands was induced in synovial fibroblasts from RA patients after stimulation with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), or interleukin-1 beta (IL-1beta). However, synovial fibroblasts significantly secreted CXCL9 and CXCL10 proteins, but not CXCL11 protein, after IFN-gamma stimulation and secreted only CXCL10 protein after TNF-alpha or IL-1beta stimulation. When stimulated with a combination of IFN-gamma and TNF-alpha, these cells were able to secrete large amounts of all three chemokines. These results indicate that synovial fibroblasts may be involved in perpetuating the Th1 immune response by producing the Th1-associated CXCR3 ligands, and the synergistic effect of IFN-gamma and TNF-alpha may be important for their chemokine production in RA joints.
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