ArticleJCI insight2019
Keratinocyte-derived IκBζ drives psoriasis and associated systemic inflammation.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 40 citations in OpenAlex.
- H2A.J is an epigenetic driver of IL-17-associated inflammation in TMolecular biomedicine · 2026Article
- Plant extract mixture shows anti-inflammatory and barrier-strengthening effects and activates aryl hydrocarbon receptor in a 2D psoriasis model.Scientific reports · 2026Article
- IL-36 mediates immune activation in Sjögren's disease and may represent a novel biomarker of disease.Journal of leukocyte biology · 2026Article
- CYLD Limits Neutrophil-Driven Psoriatic Inflammation.Inflammation · 2026Article
- Herring roe oil exerts immunomodulatory effects on the IL-17/23 signaling axis in immune and skin cells as models for psoriasis.Frontiers in medicine · 2026Article
- RIPK3 promotes skin inflammation by enhancing IL-36α signaling and necroptosis in keratinocytes.Cell death & disease · 2025Article
- Fenofibrate prevents myocardial inflammation and fibrosis via PPARα/IκBζ signaling pathway in rat autoimmune myocarditis.Experimental and therapeutic medicine · 2025Article
- Dihuangzicao Granules Regulate the AGE/RAGE/NF-κB Signaling Pathway to Inhibit Inflammation in Psoriatic MiceCombinatorial chemistry & high throughput screening · 2025Article
- The Nuclear NF-κB Regulator IκBζ: Updates on Its Molecular Functions and Pathophysiological Roles.Cells · 2024Review
- naRNA-LL37 composite DAMPs define sterile NETs as self-propagating drivers of inflammation.EMBO reports · 2024Article
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- The central inflammatory regulator IκBζ: induction, regulation and physiological functions.Frontiers in immunology · 2023Review
- IL-17A-driven psoriasis is critically dependent on IL-36 signaling.Frontiers in immunology · 2023Article
- A cutback in Imiquimod cutaneous toxicity; comparative cutaneous toxicity analysis of Imiquimod nanotransethosomal gel with 5% marketed cream on the BALB/c mice.Scientific reports · 2022Article
- Selenium-Rich Yeast Peptide Fraction Ameliorates Imiquimod-Induced Psoriasis-like Dermatitis in Mice by Inhibiting Inflammation via MAPK and NF-κB Signaling Pathways.International journal of molecular sciences · 2022Article
- Advances in the pathogenesis of psoriasis: from keratinocyte perspective.Cell death & disease · 2022Review
- Mining hidden knowledge: embedding models of cause-effect relationships curated from the biomedical literature.Bioinformatics advances · 2022Article
- IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore.Cellular and molecular life sciences : CMLS · 2021Review
- Bath Psoralen Plus UVA Therapy Suppresses Keratinocyte-Derived Chemokines in Pathogenetically Relevant Cells.JID innovations : skin science from molecules to population health · 2021Article
- Chromatin Looping Links Target Genes with Genetic Risk Loci for Dermatological Traits.The Journal of investigative dermatology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional activator IκBζ is a key regulator of psoriasis, but which cells mediate its pathogenic effect remains unknown. Here we found that IκBζ expression in keratinocytes triggers not only skin lesions but also systemic inflammation in mouse psoriasis models. Specific depletion of IκBζ in keratinocytes was sufficient to suppress the induction of imiquimod- or IL-36-mediated psoriasis. Moreover, IκBζ ablation in keratinocytes prevented the onset of psoriatic lesions and systemic inflammation in keratinocyte-specific IL-17A-transgenic mice. Mechanistically, this psoriasis protection was mediated by IκBζ deficiency in keratinocytes abrogating the induction of specific proinflammatory target genes, including Cxcl5, Cxcl2, Csf2, and Csf3, in response to IL-17A or IL-36. These IκBζ-dependent genes trigger the generation and recruitment of neutrophils and monocytes that are needed for skin inflammation. Consequently, our data uncover a surprisingly pivotal role of keratinocytes and keratinocyte-derived IκBζ as key mediators of psoriasis and psoriasis-related systemic inflammation.
Indexed as
Identifiers
What OpenQuestion holds
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.