ArticleCentral-European journal of immunology2018
IL-35 inhibits human osteoclastogenesis from monocytes induced by receptor-activator of NF-κB ligand.
Article in Central-European journal of immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- iTr35 cells: a novel immunoregulatory subset involved in bone loss in rheumatoid arthritis and clinical implications.Annals of medicine · 2025Article
- Pro-Resolving Macrophage-Induced IL-35International journal of molecular sciences · 2025Article
- Balancing the Scales: The Dual Role of Interleukins in Bone Metastatic Microenvironments.International journal of molecular sciences · 2024Review
- Osteoimmunology: The Crosstalk between T Cells, B Cells, and Osteoclasts in Rheumatoid Arthritis.International journal of molecular sciences · 2024Review
- Stimulation of Osteoclast Formation by Oncostatin M and the Role of WNT16 as a Negative Feedback Regulator.International journal of molecular sciences · 2022Review
- Elevated levels of interleukin-35 and interleukin-37 in adult patients with obstructive sleep apnea.Journal of clinical laboratory analysis · 2021Article
- Pathogenesis and Function of Interleukin-35 in Rheumatoid Arthritis.Frontiers in pharmacology · 2021Review
- Increased Interleukin-35 suppresses peripheral CD14BMC immunology · 2020Article
- IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells.International journal of molecular sciences · 2020Article
- IL-37- and IL-35/IL-37-Producing Plasma Cells in Chronic Periodontitis.Journal of dental research · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-35 is known as a regulatory cytokine produced by regulatory T cells. It has also been reported that IL-35 suppresses the proliferation of Th17 cells, which is involved in the pathogenesis of many autoimmune diseases. However, in rheumatoid arthritis patients, the role of IL-35 is controversial, and the role of IL-35 in bone metabolism has not been clarified. We investigated the effect of IL-35 on human osteoclast differentiation and activation. We first evaluated the effect of rhIL-35 on human osteoclastogenesis from monocytes cultured alone, induced by soluble-RANKL. We also examined the role of IL-35 on the bone-resorption function of mature osteoclasts. Furthermore, we analysed the molecular mechanism of IL-35 function in monocytes or pre-osteoclasts using RT-PCR. rhIL-35 significantly inhibited human osteoclastogenesis in a dose-dependent manner. In addition, rhIL-35 also significantly decreased the area of pit formation by mature osteoclasts. rhIL-35 significantly decreased mRNA expression of RANK in monocytes and RANK and FOS in pre-osteoclasts. Our current findings suggest that IL-35 inhibits osteoclastogenesis and osteoclast activation by inhibiting both RANK and FOS. IL-35 also has an inhibitory effect on osteoclastic-bone resorption, suggesting that IL-35 may have a therapeutic potential for RA.
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