ArticleOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2016
Interleukin-35 upregulates OPG and inhibits RANKL in mice with collagen-induced arthritis and fibroblast-like synoviocytes.
Article in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 26 citations in OpenAlex.
- IL-12 family cytokines and autoimmune diseases: A potential therapeutic target?Journal of translational autoimmunity · 2025Review
- Interleukin-35 pathobiology in periodontal disease: a systematic scoping review.BMC oral health · 2021Article
- Pathogenesis and Function of Interleukin-35 in Rheumatoid Arthritis.Frontiers in pharmacology · 2021Review
- Urine and serum interleukin 35 as potential biomarkers of lupus nephritis.Central-European journal of immunology · 2021Article
- IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells.International journal of molecular sciences · 2020Article
- Correlation between Serum IL-35 Levels and Bone Loss in Postmenopausal Women with Rheumatoid Arthritis.Mediators of inflammation · 2019Article
- IL-35: a new immunomodulator in autoimmune rheumatic diseases.Immunologic research · 2018Review
- IL-35 inhibits human osteoclastogenesis from monocytes induced by receptor-activator of NF-κB ligand.Central-European journal of immunology · 2018Article
- Effect of nonsurgical periodontal therapy on gingival crevicular fluid levels of Interleukin-35 in patients with periodontitis.Journal of oral biology and craniofacial researchArticle
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9 authors at 2 institutions in 1 country.
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Abstract
unlabelledIL-35 is a novel anti-inflammatory cytokine, but the exact role of IL-35 in the progression of RA remains unclear, especially associated with osteoporosis and bone erosion. The present research has not been reported. Our purpose is to study how IL-35 affects RA bone destruction.
introductionThis study investigated the effect of interleukin-35 (IL-35) on OPG and RANKL expression in collagen-induced arthritis (CIA) in rats and in cultured fibroblast-like synoviocytes (FLS).
methodsThirty DBA/1J mice were randomly assigned to three groups (n = 10 per group): the control group, the CIA group, and the CIA + IL-35 group. Collagen-induced arthritis was induced by immunization with collagen. IL-35 was intraperitoneally injected daily for 10 days, starting from the 24(th) day after immunization. FLS cells were isolated and cultured from CIA. The expression of IL-17, RANKL, and OPG was determined by RT-PCR and Western blot. Each experiment was repeated three times.
resultsCIA mice exhibited arthritis symptoms on day 24, followed by a rapid progression of arthritis. The expression of IL-17 and RANKL was increased and the expression of OPG was decreased in CIA mice compared with control mice. IL-35 treatment inhibited the development of arthritis in CIA mice, accompanied by a decrease in the expression of IL-17 and RANKL and an increase in the expression of OPG. Furthermore, IL-35 dose-dependently inhibited the expression of RANKL and increased the expression of OPG in cultured FLS cells.
conclusionIL-35 inhibits RANKL expression and increases OPG expression in CIA mice. IL-35 may be used for treating rheumatoid arthritis.
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