ArticleImmunology2014
IL-17 regulates the expressions of RANKL and OPG in human periodontal ligament cells via TRAF6/TBK1-JNK/NF-κB pathways.
Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Proteomic Biomarkers Associated with Low Bone Mineral Density: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- The dynamic landscape of T helper cell plasticity and Th17-Treg instability in periodontitis.Experimental & molecular medicine · 2026Review
- Alisol A 23,24-diacetate improves LPS-induced acute lung injury through the IL-17A/NF-κB signaling pathway.Chinese medicine · 2026Article
- IL-22 synergizes with IL-17 to promote mucosal inflammation and bone loss.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Diabetes exacerbates experimental peri-implantitis in mice with elevated IL-17A-associated inflammation and IL-17F upregulation.Scientific reports · 2026Article
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fueling bone loss: the immunometabolic reprogramming of the bone microenvironment in diabetic osteoporosis.Frontiers in immunology · 2026Review
- Removal of CD5 on T cells alters their differentiation and cytokine production in anFrontiers in immunology · 2026Article
- Crosstalk Between Hematopoietic and Mesenchymal Cells in Bone and Tooth Immune Response.Advances in experimental medicine and biology · 2026Review
- Overexpression of the IL-23/IL-17A Axis and Their Receptors (IL-23R and IL-17RA) in Gingival Tissue of Patients With Periodontitis.International journal of dentistry · 2026Article
- FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.Clinical and experimental dental research · 2025Review
- Polygenic prediction of treatment efficacy with causal transfer learning.medRxiv : the preprint server for health sciences · 2025Article
- Docosahexaenoic Acid Inhibits Osteoclastogenesis via FFAR4-Mediated Regulation of Inflammatory Cytokines.Molecules (Basel, Switzerland) · 2025Review
- Effects of chloroquine and hydroxychloroquine on bone health (Review).Molecular medicine reports · 2025Review
- Microbial dysbiosis in periodontitis and peri-implantitis: pathogenesis, immune responses, and therapeutic.Frontiers in cellular and infection microbiology · 2025Review
- Microbial dysbiosis and immune dysregulation in periodontitis and peri-implantitis.Frontiers in cellular and infection microbiology · 2025Review
- Navigating oxidative stress in oral bone regeneration: mechanisms and reactive oxygen species-regulating biomaterial strategies.Regenerative biomaterials · 2025Review
- Exploring Epigenetic Mechanisms in Aggressive Periodontitis; Unraveling the Molecular Dynamics of Disease Progression: A Narrative Review.Iranian journal of medical sciences · 2024Review
- Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review.Cureus · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-17 (IL-17 or IL-17A), a pleiotropic cytokine produced by T helper (Th) 17 cells, is involved in the pathogenesis of various autoimmune and inflammatory disorders, including periodontitis. Although the ability of pro-inflammation in periodontitis have been widely investigated, the other biological functions of IL-17, including its role in bone remodeling and the underlying molecular mechanism, have not been well clarified. In the present study, IL-17 could significantly enhance the expression of receptor activator for nuclear factor-κB ligand (RANKL) and inhibit the expression of osteoprotegerin (OPG) in human periodontal ligament cells (hPDLCs), the two critical indicators for osteoclastogenesis, suggesting IL-17 may play a destructive role in the pathogenesis of periodontal bone remodeling. Pharmaceutical signal inhibitors targeted at MAPKs, Akt or NF-κB signals, inhibited IL-17-induced RANKL and OPG regulation. Notably, the enhancement of RANKL was significantly blocked by the inhibitors of JNK and NF-κB signals. The upstream signals were further investigated with the small interfering RNA (siRNA). Both TRAF6 and TBK1 were found to be the critically signal molecules for IL-17-dependent RANKL regulation in hPDLCs. These findings may provide comprehensive understanding of the role of IL-17 in the pathogenesis of periodontitis and might also provide a reasonable way for periodontitis therapy. This article is protected by copyright. All rights reserved.
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