ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2011
Interleukin-17 synergizes with IFNγ or TNFα to promote inflammatory mediator release and intercellular adhesion molecule-1 (ICAM-1) expression in human intervertebral disc cells.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 121 citations in OpenAlex.
- Influence of interleukin 17 A and 17 F polymorphisms in keratoconus.Molecular biology reports · 2021Trial
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- Intervertebral disc progenitor cells: roles in regeneration and disease.Stem cell research & therapy · 2026Review
- From Modic changes to the disc-endplate-bone marrow complex: imaging stratification, immune remodeling, and translational implications in intervertebral disc degeneration.Frontiers in immunology · 2026Review
- What a pain in the back: etiology, diagnosis and future treatment directions for discogenic low back pain.Bone research · 2025Review
- Exploring the causal relationships between spondyloarthritis/ankylosing spondylitis and intervertebral disc degeneration: a bidirectional Mendelian randomization study.Journal of orthopaedic surgery and research · 2025Article
- Review
- Exploring the critical role of PANoptosis in the pathogenesis of intervertebral disc degeneration: mechanisms and potential therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- Immune Mechanisms and Pain in Intervertebral Disc Degeneration.Journal of inflammation research · 2025Article
- The Role of Immunocyte Infiltration Regulatory Network Based on hdWGCNA and Single-Cell Bioinformatics Analysis in Intervertebral Disc Degeneration.Inflammation · 2024Article
- Mechanism exploration of Osteoking in the treatment of lumbar disc herniation based on network pharmacology and molecular docking.Journal of orthopaedic surgery and research · 2024Article
- Etodolac utility in osteoarthritis: drug delivery challenges, topical nanotherapeutic strategies and potential synergies.Therapeutic delivery · 2024Review
- Integrated analysis of single-cell and bulk RNA sequencing data identifies the characteristics of ferroptosis in lumbar disc herniation.Functional & integrative genomics · 2023Article
- Intervertebral disc degeneration and inflammatory microenvironment: expression, pathology, and therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Cytokine Imbalance as a Biomarker of Intervertebral Disk Degeneration.International journal of molecular sciences · 2023Review
- Regulatory Effect of Inflammatory Mediators in Intervertebral Disc Degeneration.Mediators of inflammation · 2023Review
- Should Degenerated Intervertebral Discs of Patients with Modic Type 1 Changes Be Treated with Mesenchymal Stem Cells?International journal of molecular sciences · 2022Review
- Innovative immune mechanisms and antioxidative therapies of intervertebral disc degeneration.Frontiers in bioengineering and biotechnology · 2022Review
- Melatonin reverses tumor necrosis factor-alpha-induced metabolic disturbance of human nucleus pulposus cells via MTNR1B/Gαi2/YAP signaling.International journal of biological sciences · 2022Article
- The Role of IL-17-Mediated Inflammatory Processes in the Pathogenesis of Intervertebral Disc Degeneration and Herniation: A Comprehensive Review.Frontiers in cell and developmental biology · 2022Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Interleukin-17 (IL-17) is a cytokine recently shown to be elevated, along with interferon-γ (IFNγ) and tumor necrosis factor (TNFα), in degenerated and herniated intervertebral disc (IVD) tissues, suggesting a role for these cytokines in intervertebral disc disease. The objective of our study was to investigate the involvement of IL-17 and costimulants IFNγ and TNFα in intervertebral disc pathology. Cells were isolated from anulus fibrosus and nucleus pulposus tissues of patients undergoing surgery for intervertebral disc degeneration or scoliosis. The production of inflammatory mediators, nitric oxide (NOx), prostaglandin E2 (PGE2) and interleukin-6 (IL-6), as well as intercellular adhesion molecule (ICAM-1) expression, were quantified for cultured cells following exposure to IL-17, IFNγ, and TNFα. Intervertebral disc cells exposed to IL-17, IFNγ, or TNFα showed a remarkable increase in inflammatory mediator release and ICAM-1 expression (GLM and ANOVA, p < 0.05). Addition of IFNγ or TNFα to IL-17 demonstrated a synergistic increase in inflammatory mediator release, and a marked increase in ICAM-1 expression. These findings suggest that IVD cells not only respond with a catabolic phenotype to IL-17 and costimulants IFNγ and TNFα, but also express surface ligands with consequent potential to recruit additional lymphocytes and immune cells to the IVD microenvironment. IL-17 may be an important regulator of inflammation in the IVD pathologies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.