ReviewCells2020
Decoding IL-23 Signaling Cascade for New Therapeutic Opportunities.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 87 citations in OpenAlex.
- Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.Clinical reviews in allergy & immunology · 2026Review
- Harnessing Natural Compounds in Psoriasis: Targeting Cellular Pathways for Effective Therapy.Phytotherapy research : PTR · 2026Review
- Novel Therapeutic Strategies and Biomarkers in the Management of Inflammatory Bowel Disease: A Narrative Review.Cureus · 2026Review
- Inflame and restrain - the paradoxical roles of IL-12 and IL-23 in immunity.Nature reviews. Immunology · 2026Review
- Intracellular IL-23R is necessary for mitotic spindle formation and viability in AML.Leukemia · 2026Article
- Wogonin attenuates psoriasis through anti-inflammatory effects by inhibiting reactive oxygen species production and the AKT/NF-κB signaling pathway.Scientific reports · 2026Article
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- Regulation and Interaction Among SOCS1 and SOCS3 by MicroRNAs in Multiple Sclerosis: A Review andThe Yale journal of biology and medicine · 2026Review
- NGO ameliorates psoriasis by modulating mitochondrial function and suppressing pSTAT3-IL-17-expressing CD8Journal of nanobiotechnology · 2026Article
- Receptor engineering constitutes feedback control and robustness of IL-23R signaling and highlights importance of intracellular cytokine receptor signaling motifs.Cell communication and signaling : CCS · 2026Article
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.Frontiers in immunology · 2026Article
- Biologic and targeted synthetic therapies in ankylosing spondylitis: a pharmacological review.Frontiers in pharmacology · 2026Review
- Differential Transcriptomic Features of Peripheral Blood Mononuclear Cells in Pulmonary Sarcoidosis with and Without Extrapulmonary Lesions in an East Asian Population.Biomedicines · 2025Article
- Targeting the JAK/STAT pathway in palmoplantar pustulosis: a review.Annals of medicine · 2025Review
- Efficacy of Probiotic Supplementation in the Management of Psoriasis: A Systematic Review.Cureus · 2025Review
- ECM-Induced IL-23 Drives Immune Suppression in Breast Cancer via Regulating PD-1 on Tregs.Journal of experimental & clinical cancer research : CR · 2025Article
- Association of skin microbiome with interleukin-23 in patients with plaque psoriasis.Postepy dermatologii i alergologii · 2025Article
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.bioRxiv : the preprint server for biology · 2025Article
- SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation.Immune network · 2025Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interleukin 23 (IL-23) is a key pro-inflammatory cytokine in the development of chronic inflammatory diseases, such as psoriasis, inflammatory bowel diseases, multiple sclerosis, or rheumatoid arthritis. The pathological consequences of excessive IL-23 signaling have been linked to its ability to promote the production of inflammatory mediators, such as IL-17, IL-22, granulocyte-macrophage colony-stimulating (GM-CSF), or the tumor necrosis factor (TNFα) by target populations, mainly Th17 and IL-17-secreting TCRγδ cells (Tγδ17). Due to their pivotal role in inflammatory diseases, IL-23 and its downstream effector molecules have emerged as attractive therapeutic targets, leading to the development of neutralizing antibodies against IL-23 and IL-17 that have shown efficacy in different inflammatory diseases. Despite the success of monoclonal antibodies, there are patients that show no response or partial response to these treatments. Thus, effective therapies for inflammatory diseases may require the combination of multiple immune-modulatory drugs to prevent disease progression and to improve quality of life. Alternative strategies aimed at inhibiting intracellular signaling cascades using small molecule inhibitors or interfering peptides have not been fully exploited in the context of IL-23-mediated diseases. In this review, we discuss the current knowledge about proximal signaling events triggered by IL-23 upon binding to its membrane receptor to bring to the spotlight new opportunities for therapeutic intervention in IL-23-mediated 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.