ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Dual Inhibition of TNFR1 and IFNAR1 in Imiquimod-Induced Psoriasiform Skin Inflammation in Mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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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
26 citing papers in PubMed, 43 citations in OpenAlex.
- Topical ronomilast alone or combined with clobetasol ameliorates imiquimod-induced psoriasis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- SPT6 maintains epidermal homeostasis by inhibiting an NF-κB-positive feedback loop to prevent excessive inflammation.Cellular & molecular immunology · 2026Article
- Traditional medicine meets modern science: Halofuginone's role in combating autoimmune diseases.Journal of natural medicines · 2025Review
- Systemic IFN-I combined with topical TLR7/8 agonists promotes distant tumor suppression by c-Jun-dependent IL-12 expression in dendritic cells.Nature cancer · 2025Article
- Article
- Granzyme K mediates IL-23-dependent inflammation and keratinocyte proliferation in psoriasis.Frontiers in immunology · 2024Article
- TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.Nature communications · 2023Article
- TNF and TNF receptors as therapeutic targets for rheumatic diseases and beyond.Nature reviews. Rheumatology · 2023Review
- CD1a promotes systemic manifestations of skin inflammation.Nature communications · 2022Article
- The Therapeutic Effect of Tacrolimus in a Mouse Psoriatic Model is Associated with the Induction of Myeloid-derived Suppressor Cells.Rheumatology and immunology research · 2022Article
- IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation.The Journal of investigative dermatology · 2022Article
- OTULIN maintains skin homeostasis by controlling keratinocyte death and stem cell identity.Nature communications · 2021Article
- IL-1 Family Antagonists in Mouse and Human Skin Inflammation.Frontiers in immunology · 2021Review
- Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection.Immunity · 2020Article
- IL-36 signaling in keratinocytes controls early IL-23 production in psoriasis-like dermatitis.Life science alliance · 2020Article
- Novel and Modified Neutrophil Elastase Inhibitor Loaded in Topical Formulations for Psoriasis Management.Pharmaceutics · 2020Article
- Article
- Alleviation of Ultraviolet-B Radiation-Induced Photoaging by a TNFR Antagonistic Peptide, TNFR2-SKE.Molecules and cells · 2019Article
- Therapeutic Implication of SOCS1 Modulation in the Treatment of Autoimmunity and Cancer.Frontiers in pharmacology · 2019Review
- A requirement for slc15a4 in imiquimod-induced systemic inflammation and psoriasiform inflammation in mice.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory skin disease affecting 2-3% of the world population and is mainly characterized by epidermal hyperplasia, scaling, and erythema. A prominent role for TNF in the pathogenesis of psoriasis has been shown, and consequently various types of TNF antagonists such as etanercept and infliximab have been used successfully. Recently, increasing amounts of data suggest that type I IFNs are also crucial mediators of psoriasis. To investigate whether blocking their respective receptors would be useful, TNFR1- and IFNAR1-deficient mice were challenged with Aldara, which contains imiquimod, and is used as an experimental model to induce psoriasis-like skin lesions in mice. Both transgenic mice showed partial protection toward Aldara-induced inflammation compared with control groups. Additionally, TNFR1 knockout mice showed sustained type I IFN production in response to Aldara. Double knockout mice lacking both receptors showed superior protection to Aldara in comparison with the single knockout mice and displayed reduced levels of IL-12p40, IL-17F, and S100A8, indicating that the TNF and type I IFN pathways contribute significantly to inflammation upon treatment with Aldara. Our findings reveal that dual inhibition of TNFR1 and IFNAR1 may represent a potential novel strategic treatment of psoriasis.
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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.