ArticleFrontiers in immunology2017
Interleukin-25 Produced by Synoviocytes Has Anti-inflammatory Effects by Acting As a Receptor Antagonist for Interleukin-17A Function.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- IL-25-ILC2-IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity.Journal of neuroinflammation · 2026Article
- Role of Interleukin-17 family cytokines in disease severity of patients with knee osteoarthritis.Advances in rheumatology (London, England) · 2024Article
- New insights into the function of Interleukin-25 in disease pathogenesis.Biomarker research · 2023Review
- Inflammatory Arthritis and Bone Metabolism Regulated by Type 2 Innate and Adaptive Immunity.International journal of molecular sciences · 2022Review
- Interleukin 25 and its biological features and function in intestinal diseases.Central-European journal of immunology · 2022Review
- The Th17 Pathway in Vascular Inflammation: Culprit or Consort?Frontiers in immunology · 2022Review
- Exploring the Diverse Immune and Genetic Landscape of Psoriatic Arthritis.Journal of clinical medicine · 2021Review
- Local and systemic effects of IL-17 in joint inflammation: a historical perspective from discovery to targeting.Cellular & molecular immunology · 2021Review
- Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications.Frontiers in immunology · 2021Review
- Roles of IL-25 in Type 2 Inflammation and Autoimmune Pathogenesis.Frontiers in immunology · 2021Review
- Role of Interleukin-17 in Acute Pancreatitis.Frontiers in immunology · 2021Review
- Evaluation of the Effects of 1,25VitD3 on Inflammatory Responses and IL-25 Expression.Frontiers in genetics · 2021Article
- Interleukin (IL)-25 suppresses IL-22-induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway.Arthritis research & therapy · 2020Article
- The expression of interleukin-25 increases in human coronary artery disease and is associated with the severity of coronary stenosis.Anatolian journal of cardiology · 2020Article
- The Roles of Lipoprotein in Psoriasis.International journal of molecular sciences · 2020Review
- Synergistic Interaction Between High Bioactive IL-17A and Joint Destruction for the Occurrence of Cardiovascular Events in Rheumatoid Arthritis.Frontiers in immunology · 2020Article
- Systemic effects of IL-17 in inflammatory arthritis.Nature reviews. Rheumatology · 2019Review
- IL-17 in Rheumatoid Arthritis and Precision Medicine: From Synovitis Expression to Circulating Bioactive Levels.Frontiers in medicine · 2018Review
- IL-25 dampens the growth of human germinal center-derived B-cell non Hodgkin Lymphoma by curtailing neoangiogenesis.OncoimmunologyArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The production and function of cytokines are highly regulated. One mechanism is the balance between pro- and anti-inflammatory cytokines. As interleukin (IL)-17A and IL-25 share the IL-17RA receptor chain, we hypothesize that IL-25 acts as an IL-17A receptor antagonist and limits its pro-inflammatory effects. The production and expression kinetics of IL-25 and its receptor chains IL-17RA and RB were analyzed in rheumatoid synoviocytes alone or in coculture with peripheral blood mononuclear cells (PBMCs). The effects of autocrine or exogenous IL-25 on synoviocytes were investigated in the presence or not of an anti-IL-25 antibody. To study the regulatory effects of IL-25, synoviocytes and/or PBMCs were exposed to IL-25 before being treated with IL-17A and tumor necrosis factor alpha (TNF-α) alone or combined. IL-25, IL-6, and bioactive IL-17A were quantified in rheumatoid arthritis (RA) patient plasma. Synoviocytes expressed and secreted IL-25, and expressed the two chains of its receptor IL-17RA and IL-17RB. IL-17RB expression was increased by TNF-α. IL-25 production occurred at a delayed time point (5 days) after stimulation with IL-17A and TNF-α. Synoviocytes pretreated with IL-25 were less responsive to IL-17A and TNF-α. PBMCs exposed to IL-25 showed a decreased production of pro-inflammatory mediators, including IL-17A with a 57% decrease;
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