ReviewEuropean journal of immunology2018
The role of IL-23 receptor signaling in inflammation-mediated erosive autoimmune arthritis and bone remodeling.
Review in 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 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Trial
- Cytokine multimerization: when more is more and sometimes less.Nature reviews. Immunology · 2026Review
- Association ofGenes · 2025Article
- The genetic puzzle of rheumatoid arthritis: Causes, progression, and treatment.Biochemistry and biophysics reports · 2025Review
- Cardiometabolic Risk in Psoriatic Arthritis: A Hidden Burden of Inflammation and Metabolic Dysregulation.Metabolites · 2025Review
- Low-Intensity Pulsed Ultrasound Promotes a Treg-Like Phenotype and Suppresses a Th17-Like Phenotype in CD4Journal of inflammation research · 2025Article
- Article
- Osteoarthritis versus psoriasis arthritis: Physiopathology, cellular signaling, and therapeutic strategies.Genes & diseases · 2024Review
- Biology and therapeutic potential of mesenchymal stem cell extracellular vesicles in axial spondyloarthritis.Communications biology · 2023Review
- Identifying hub genes and miRNAs in Crohn's disease by bioinformatics analysis.Frontiers in genetics · 2022Article
- IL-23 orchestrating immune cell activation in arthritis.Rheumatology (Oxford, England) · 2021Article
- IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation.Scientific reports · 2021Article
- Role of the IL23/IL17 Pathway in Crohn's Disease.Frontiers in immunology · 2021Review
- Expression Profile of Osteoclasts Following the Stimulation With Interleukin-23 in Mice.Archives of rheumatology · 2020Article
- CD4European journal of immunology · 2020Article
- Responses to Cytokine Inhibitors Associated with Cellular Composition in Models of Immune-Mediated Inflammatory Arthritis.ACR open rheumatology · 2020Article
- Effects of the IL-23-IL-17 pathway on bone in spondyloarthritis.Nature reviews. Rheumatology · 2018Review
- p19-Targeting ILP Protein Blockers of IL-23/Th-17 Pro-Inflammatory Axis Displayed on Engineered Bacteria of Food Origin.International journal of molecular sciences · 2018Article
Corrections and comments
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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 IL-23/Th17 axis has been implicated in the development of autoimmune diseases, such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). RA and PsA are heterogeneous diseases with substantial burden on patients. Increasing evidence suggests that the IL-23 signaling pathway may be involved in the development of autoimmunity and erosive joint damage. IL-23 can act either directly or indirectly on bone forming osteoblasts as well as on bone resorbing osteoclasts. As IL-23 regulates the activity of cells of the bone, it is conceivable that in addition to inflammation-mediated joint erosion, IL-23 may play a role in physiological bone remodeling. In this review, we focus on the role of IL-23 in autoimmune arthritis in patients and murine models, and provide an overview of IL-23 producing and responding cells in autoimmune arthritic joints. In addition, we discuss the role of IL-23 on bone forming osteoblasts and bone resorbing osteoclasts regarding inflammation-mediated joint damage and bone remodeling. At last, we briefly discuss the clinical implications of targeting this pathway for joint damage and systemic bone loss in autoimmune arthritis.
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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.