ArticleArthritis research & therapy2009
Human rheumatoid arthritis tissue production of IL-17A drives matrix and cartilage degradation: synergy with tumour necrosis factor-alpha, Oncostatin M and response to biologic therapies.
Article in Arthritis research & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 166 citations in OpenAlex.
- Regulatory Effect of Iguratimod on the Balance of Th Subsets and Inhibition of Inflammatory Cytokines in Patients with Rheumatoid Arthritis.Mediators of inflammation · 2015Trial
- The Pathophysiological Significance of Dual Inhibition of IL-17A and IL-17F in Psoriatic Arthritis and Axial Spondyloarthritis.Mediterranean journal of rheumatology · 2026Review
- IL-23 and monocyte interactions redirect human Th17.1 cells to an IL-17AFrontiers in immunology · 2026Article
- Comprehensive Profiling of Cytokines and Growth Factors: Pathogenic Roles and Clinical Applications in Autoimmune Diseases.International journal of molecular sciences · 2025Review
- Potential of Alkaloids fromCurrent issues in molecular biology · 2025Article
- Targeting rheumatoid arthritis: a molecular perspective on biologic therapies and clinical progress.Journal of biological engineering · 2025Review
- Evaluating the inhibition of IL-17A and TNFα in a cartilage explant model cultured with Th17-derived cytokines.Journal of translational autoimmunity · 2024Article
- Natural Product-Derived Compounds Targeting Keratinocytes and Molecular Pathways in Psoriasis Therapeutics.International journal of molecular sciences · 2024Review
- Network-based cytokine inference implicates Oncostatin M as a driver of an inflammation phenotype in knee osteoarthritis.Aging cell · 2024Article
- Distinct fibroblast functions associated with fibrotic and immune-mediated inflammatory diseases and their implications for therapeutic development.F1000Research · 2024Review
- Site of invasion revisited: epigenetic drivers of joint destruction in RA.Annals of the rheumatic diseases · 2023Review
- T Helper 17-Like Regulatory T Cells in Equine Synovial Fluid Are Associated With Disease Severity of Naturally Occurring Posttraumatic Osteoarthritis.The American journal of sports medicine · 2023Article
- Immunomodulatory role of T helper cells in rheumatoid arthritis : a comprehensive research review.Bone & joint research · 2022Article
- Plasma interleukin-23 and circulating IL-17AArthritis research & therapy · 2022Article
- Metformin and its therapeutic applications in autoimmune inflammatory rheumatic disease.The Korean journal of internal medicine · 2022Review
- Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis.Journal of immunology research · 2022Review
- Inside the Joint of Inflammatory Arthritis Patients: Handling and Processing of Synovial Tissue Biopsies for High Throughput Analysis.Frontiers in medicine · 2022Review
- IL-23/IL-17 axis and soluble receptors isoforms sIL-23R and sIL-17RA in patients with rheumatoid arthritis-presenting periodontitis.Journal of clinical laboratory analysis · 2021Observational
- Regulatory T cells provide chondroprotection through increased TIMP1, IL-10 and IL-4, but cannot mitigate the catabolic effects of IL-1β and IL-6 in a tri-culture model of osteoarthritis.Osteoarthritis and cartilage open · 2021Article
- Navigating the diverse immune landscapes of psoriatic arthritis.Seminars in immunopathology · 2021Review
30 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe aim of this study was to examine IL-17A in patients, following anti-TNF-alpha therapy and the effect of IL-17A on matrix turnover and cartilage degradation.
methodsIL-17A expression was examined by ELISA and immunohistology in the rheumatoid arthritis (RA) joints. RA whole synovial tissue explant (RA ST), primary synovial fibroblasts (RASFC), human cartilage and chondrocyte cultures were stimulated with IL-17A +/- TNF-alpha and Oncostatin M (OSM). Matrix metalloproteinase (MMP) and tissue inhibitor (TIMP-1) were assessed by ELISA and zymography. Cartilage proteoglycan release was assessed histologically by Safranin-O staining. Clinical parameters, IL-17A, MMP/TIMP were assessed in patients pre/post biologic therapy.
resultsIL-17A levels were higher in RA vs osteoarthritis (OA)/normal joints (P < 0.05). IL-17A up-regulated MMP-1, -2, -9, and -13 in RA ST, RASFC, cartilage and chondrocyte cultures (P < 0.05). In combination with TNF-alpha and OSM, IL-17A shifted the MMP:TIMP-1 ratio in favor of matrix degradation (all P < 0.05). Cartilage proteoglycan depletion in response to IL-17A was mild; however, in combination with TNF-alpha or OSM showed almost complete proteoglycan depletion. Serum IL-17A was detected in 28% of patients commencing biologic therapy. IL-17A negative patients demonstrated reductions post therapy in serum MMP1/TIMP4, MMP3/TIMP1 and MMP3/TIMP4 ratios and an increase in CS846 (all P < 0.05). No significant changes were observed in IL-17A positive patients.
conclusionsIL-17A is produced locally in the inflamed RA joint. IL-17A promotes matrix turnover and cartilage destruction, especially in the presence of other cytokines, mimicking the joint environment. IL-17A levels are modulated in vivo, following anti-TNF therapy, and may reflect changes in matrix turnover.
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