ArticlePloS one2013
Suppression of molecular inflammatory pathways by Toll-like receptor 7, 8, and 9 antagonists in a model of IL-23-induced skin inflammation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Meta-analysis derived atopic dermatitis (MADAD) transcriptome defines a robust AD signature highlighting the involvement of atherosclerosis and lipid metabolism pathways.BMC medical genomics · 2015Pooled it
- Does imiquimod pretreatment optimize 308-nm excimer laser (UVB) therapy in psoriasis patients?Photodermatology, photoimmunology & photomedicine · 2017Trial
- Reevaluating the Imiquimod Model: A Barrier to Translational Progress in Psoriasis.The Journal of investigative dermatology · 2026Review
- Ferroptosis of select skin epithelial cells initiates and maintains chronic systemic immune-mediated psoriatic disease.The Journal of clinical investigation · 2024Article
- Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.Current treatment options in rheumatology · 2023Article
- Recent Advances on Small-Molecule Antagonists Targeting TLR7.Molecules (Basel, Switzerland) · 2023Review
- Application and prospect of targeting innate immune sensors in the treatment of autoimmune diseases.Cell & bioscience · 2022Review
- The Dendritic Cell Dilemma in the Skin: Between Tolerance and Immunity.Frontiers in immunology · 2022Review
- Nucleic acid-sensing toll-like receptors: Important players in Sjögren's syndrome.Frontiers in immunology · 2022Review
- Toll-like receptors, innate immune system, and lung diseases: a vital trilateral association.EXCLI journal · 2022Article
- Crossing the boundaries: IL-23 and its role in linking inflammation of the skin, gut and joints.Rheumatology (Oxford, England) · 2021Article
- IRAK4 inhibition: a promising strategy for treating RA joint inflammation and bone erosion.Cellular & molecular immunology · 2021Article
- Pattern recognition receptors in health and diseases.Signal transduction and targeted therapy · 2021Review
- Dendritic Cells and CCR7 Expression: An Important Factor for Autoimmune Diseases, Chronic Inflammation, and Cancer.International journal of molecular sciences · 2021Review
- Role of the Innate Immunity Signaling Pathway in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2021Review
- Role of pattern recognition receptors and the microbiota in neurological disorders.The Journal of physiology · 2021Article
- Immune responses and therapeutic options in psoriasis.Cellular and molecular life sciences : CMLS · 2021Review
- The role of Langerhans cells in epidermal homeostasis and pathogenesis of psoriasis.Journal of cellular and molecular medicine · 2020Review
- CARD14eLife · 2020Article
- Agonist and antagonist ligands of toll-like receptors 7 and 8: Ingenious tools for therapeutic purposes.European journal of medicinal chemistry · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a complex inflammatory disease resulting from the activation of T helper (Th) 1 and Th17 cells. Recent evidence suggests that abnormal activation of Toll-like receptors (TLRs) 7, 8 and 9 contributes to the initiation and maintenance of psoriasis. We have evaluated the effects of TLR antagonists on the gene expression profile in an IL-23-induced skin inflammation model in mice. Psoriasis-like skin lesions were induced in C57BL/6 mice by intradermal injection of IL-23 in the dorsum. Two TLR antagonists were compared: IMO-3100, an antagonist of TLRs 7 and 9, and IMO-8400, an antagonist of TLRs 7, 8 and 9, both of which previously have been shown to reduce epidermal hyperplasia in this model. Skin gene expression profiles of IL-23-induced inflammation were compared with or without TLR antagonist treatment. IL-23 injection resulted in alteration of 5100 gene probes (fold change ≥ 2, FDR < 0.05) including IL-17 pathways that are up-regulated in psoriasis vulgaris. Targeting TLRs 7, 8 and 9 with IMO-8400 resulted in modulation of more than 2300 mRNAs while targeting TLRs 7 and 9 with IMO-3100 resulted in modulation of more than 1900 mRNAs. Both agents strongly decreased IL-17A expression (>12-fold reduction), normalized IL-17 induced genes such as beta-defensin and CXCL1, and normalized aberrant expression of keratin 16 (indicating epidermal hyperplasia). These results suggest that IL-23-driven inflammation in mouse skin may be dependent on signaling mediated by TLRs 7, 8, and 9 and that these receptors represent novel therapeutic targets in psoriasis vulgaris and other diseases with similar pathophysiology.
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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.