ArticleInternational journal of molecular sciences2020
IL-24 Negatively Regulates Keratinocyte Differentiation Induced by Tapinarof, an Aryl Hydrocarbon Receptor Modulator: Implication in the Treatment of Atopic Dermatitis.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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
29 citing papers in PubMed, 46 citations in OpenAlex.
- Rethinking Head and Neck Atopic Dermatitis: Pathogenic Axes and Emerging Therapeutic Directions.American journal of clinical dermatology · 2026Review
- From Barrier Disruption and Immune Dysregulation to Targeted Therapies in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2026Review
- The Therapeutic Effect of Tapinarof on In Vitro Cutaneous Lupus-like Keratinocyte Model.International journal of molecular sciences · 2026Article
- Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- STAT3 ablation in keratinocytes ameliorates allergic contact dermatitis in DNCB-induced mice model.Iranian journal of basic medical sciences · 2026Article
- Interleukin-24 in type 2 immune diseases.Frontiers in immunology · 2026Review
- The dual roles of T cells and keratinocytes in seborrheic dermatitis: a narrative review.European journal of medical research · 2025Review
- Harnessing Quinone Derivatives fromACS pharmacology & translational science · 2025Article
- Advancements in pharmacological interventions for atopic dermatitis current strategies and future directions.Inflammopharmacology · 2025Review
- Benvitimod upregulates filaggrin, involucrin and loricrin expressions via aryl hydrocarbon receptor-OVO-like 1 axis.Archives of dermatological research · 2024Article
- Induction of Semaphorin 3A by Resveratrol and Pinostilbene via Activation of the AHR-NRF2 Axis in Human Keratinocytes.Antioxidants (Basel, Switzerland) · 2024Article
- Atopic Dermatitis and Psoriasis: Similarities and Differences in Metabolism and Microbiome.Clinical reviews in allergy & immunology · 2024Review
- Regulatory Mechanism of the IL-33-IL-37 Axis via Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis.International journal of molecular sciences · 2023Review
- Environmental Air Pollutants Affecting Skin Functions with Systemic Implications.International journal of molecular sciences · 2023Review
- Multi-Omics Research Strategies for Psoriasis and Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Novel Therapeutic Targets for the Treatment of Atopic Dermatitis.Biomedicines · 2023Review
- Hochuekkito exerts the anti-allergic effects via activating regulatory T cells in a murine model of contact hypersensitivity.Journal of natural medicines · 2023Article
- IL-24 Contributes to Neutrophilic Asthma in an IL-17A-Dependent Manner and Is Suppressed by IL-37.Allergy, asthma & immunology research · 2022Article
- Carboxamide Derivatives Are Potential Therapeutic AHR Ligands for Restoring IL-4 Mediated Repression of Epidermal Differentiation Proteins.International journal of molecular sciences · 2022Article
- Molecular and cellular mechanisms of itch and pain in atopic dermatitis and implications for novel therapeutics.Clinical & translational immunology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Skin barrier dysfunction, including reduced filaggrin (FLG) and loricrin (LOR) expression, plays a critical role in atopic dermatitis (AD) development. Since aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, mediates keratinocyte differentiation, it is a potential target for AD treatment. Recently, clinical studies have shown that tapinarof, an AHR modulator, attenuated the development of AD. To examine the molecular mechanism involved in this, we analyzed tapinarof-treated normal human epidermal keratinocytes (NHEKs). Tapinarof upregulated FLG and LOR mRNA and protein expression in an AHR-dependent manner. Tapinarof also induced the secretion of IL-24, a cytokine that activates Janus kinase (JAK)-signal transducer and activator of transcription (STAT), leading to the downregulation of FLG and LOR expression. Knockdown of either IL-24 or STAT3 expression by small interfering RNA (siRNA) transfection augmented the upregulation of FLG and LOR expression induced by tapinarof, suggesting that inhibition of the IL-24/STAT3 axis during AHR activation supports the improvement of skin barrier dysfunction. Furthermore, tapinarof alone could restore the downregulation of FLG and LOR expression induced by IL-4, a key cytokine of AD, and its combination with JAK inhibitors enhanced this effect. These findings provide a new strategy for treating AD using AHR modulators and JAK inhibitors.
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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.