ArticleArthritis research & therapy2020
Interleukin (IL)-25 suppresses IL-22-induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway.
Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Trial
- TLR4-dependent upregulation of IL-22-producing T cells in the bone niche links to the imbalance of bone homeostasis.Cellular & molecular biology letters · 2026Article
- Diabetic Charcot Neuroarthropathy: A Contemporary Review of Molecular and Genetic Markers.Foot & ankle international · 2026Review
- Mechanistic Study of Yibi Decoction in Treating Rheumatoid ArthritisEndocrine, metabolic & immune disorders drug targets · 2026Article
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- Target Role of Monocytes as Key Cells of Innate Immunity in Rheumatoid Arthritis.Diseases (Basel, Switzerland) · 2024Review
- Innate Type-2 Cytokines: From Immune Regulation to Therapeutic Targets.Immune network · 2024Review
- Role of Interleukin-17 family cytokines in disease severity of patients with knee osteoarthritis.Advances in rheumatology (London, England) · 2024Article
- ADAM8 silencing suppresses the migration and invasion of fibroblast-like synoviocytes via FSCN1/MAPK cascade in osteoarthritis.Arthritis research & therapy · 2024Article
- Endothelial Stat3 activation promotes osteoarthritis development.Cell proliferation · 2023Article
- Exogenous IL-25 ameliorates airway neutrophilia via suppressing macrophage M1 polarization and the expression of IL-12 and IL-23 in asthma.Respiratory research · 2023Article
- CD4+ T-cell subsets in autoimmune hepatitis: A review.Hepatology communications · 2023Review
- Ixekizumab for brodalumab-induced articular involvement in psoriatic arthritis: beyond IL-17A inhibition.Rheumatology international · 2023Article
- Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment.International journal of molecular sciences · 2023Review
- New insights into the function of Interleukin-25 in disease pathogenesis.Biomarker research · 2023Review
- Leveraging mice with diverse microbial exposures for advances in osteoimmunology.Frontiers in endocrinology · 2023Article
- DJ-1 controls T cell differentiation and osteoclastogenesis in rheumatoid arthritis.Scientific reports · 2022Article
- Targeting the Epithelium-Derived Innate Cytokines: From Bench to Bedside.Immune network · 2022Review
- Inflammatory Arthritis and Bone Metabolism Regulated by Type 2 Innate and Adaptive Immunity.International journal of molecular sciences · 2022Review
- The Roles of IL-22 and Its Receptor in the Regulation of Inflammatory Responses in the Brain.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe present study aimed to evaluate the suppressive role of interleukin (IL)-25 in IL-22-induced osteoclastogenesis and receptor activator of nuclear factor κB ligand (RANKL) expression in rheumatoid arthritis (RA).
methodsSerum from patients with RA and osteoarthritis (OA), and healthy controls, and synovial fluid from patients with RA and OA were collected, and the levels of IL-22 and IL-25 were measured. RA and OA synovial tissues were stained against IL-25. Fibroblast-like synoviocytes (FLSs) of patients with RA were cultured with IL-22, in the presence or absence of IL-25, and RANKL expression was measured by real-time PCR and enzyme-linked immunosorbent assay (ELISA). Human peripheral blood monocytes were cultured under IL-22/RANKL + M-CSF, with or without IL-25, and tartrate-resistant acid phosphatase (TRAP)-positive cells and osteoclast-related markers were investigated to determine osteoclastogenesis.
resultsSerum and synovial IL-25 levels in RA were upregulated compared to those in OA and healthy control, and elevated expression of IL-25 in RA synovial tissue was re-confirmed. IL-25 and IL-22 levels showed significant correlation in serum and synovial fluid. Pre-treatment of FLS with IL-25 reduced IL-22-induced RANKL expression at the RNA level. The suppressive effects of IL-25 were confirmed to occur through the STAT3 and p38 MAPK/IκBα pathways. IL-25 reduced osteoclast differentiation and suppressed the expression of osteoclast-related markers.
conclusionIn the current study, we demonstrated the regulatory effect of IL-25 on IL-22-induced osteoclastogenesis. Therapeutic approach involving augmentation of IL-25 regulatory response may serve as a novel treatment option for RA, especially by suppressing osteoclastogenesis.
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