ArticleInternational journal of molecular sciences2018
Glyteer, Soybean Tar, Impairs IL-4/Stat6 Signaling in Murine Bone Marrow-Derived Dendritic Cells: The Basis of Its Therapeutic Effect on Atopic Dermatitis.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Mast cell-neuron axis as a core mechanism in chronic pruritus of atopic dermatitis: from mechanistic insights to therapeutic targets.Frontiers in immunology · 2025Review
- Natural Products as Modulators of Aryl Hydrocarbon Receptor Signaling in Atopic Dermatitis Management.Molecules (Basel, Switzerland) · 2024Review
- Identification of novel hub genes and immune infiltration in atopic dermatitis using integrated bioinformatics analysis.Scientific reports · 2024Article
- Article
- Tryptophan, an important link in regulating the complex network of skin immunology response in atopic dermatitis.Frontiers in immunology · 2023Review
- Potential Therapeutic Skin Microbiomes SuppressingInternational journal of molecular sciences · 2022Article
- Potential Natural Biomolecules Targeting JAK/STAT/SOCS Signaling in the Management of Atopic Dermatitis.Molecules (Basel, Switzerland) · 2022Review
- A New Insight into the Potential Role of Tryptophan-Derived AhR Ligands in Skin Physiological and Pathological Processes.International journal of molecular sciences · 2021Review
- Committed Human CD23-Negative Light-Zone Germinal Center B Cells Delineate Transcriptional Program Supporting Plasma Cell Differentiation.Frontiers in immunology · 2021Article
- Regulation of Skin Barrier Function via Competition between AHR Axis versus IL-13/IL-4‒JAK‒STAT6/STAT3 Axis: Pathogenic and Therapeutic Implications in Atopic Dermatitis.Journal of clinical medicine · 2020Review
- Regulation of Filaggrin, Loricrin, and Involucrin by IL-4, IL-13, IL-17A, IL-22, AHR, and NRF2: Pathogenic Implications in Atopic Dermatitis.International journal of molecular sciences · 2020Review
- Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1.Journal of clinical medicine · 2020Article
- Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis.International journal of molecular sciences · 2019Review
- IL-4 Augments IL-31/IL-31 Receptor Alpha Interaction Leading to Enhanced Ccl 17 and Ccl 22 Production in Dendritic Cells: Implications for Atopic Dermatitis.International journal of molecular sciences · 2019Article
- Genome-Wide Transcriptional Analysis Reveals Novel AhR Targets That Regulate Dendritic Cell Function during Influenza A Virus Infection.ImmunoHorizons · 2019Article
- Dendritic Cell-Mediated Th2 Immunity and Immune Disorders.International journal of molecular sciences · 2019Review
- Myeloid-Derived Suppressor Cells as a Regulator of Immunity in Organ Transplantation.International journal of molecular sciences · 2018Review
- The role of NRF2 transcription factor in inflammatory skin diseases.BioFactors (Oxford, England)Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a common inflammatory skin disease. Recent studies have revealed the involvement of T helper (Th)2 cytokines including Interleukin 4 (IL-4) in the pathogenesis of AD. Since epidermal Langerhans cells (LCs) and dermal myeloid dendritic cells (DCs) produce CCL17 and CCL22 that chemoattract Th2 cells, interfering with CCL17 and CCL22 production from LCs and dermal myeloid DCs may be beneficial in the treatment of AD. To investigate this, we stimulated murine bone marrow-derived DCs (BMDCs) with IL-4. IL-4 stimulation produced Ccl17 and Ccl22, which was attenuated by soybean tar Glyteer, a known aryl hydrocarbon receptor (Ahr) activator. Notably, Glyteer treatment blocked the nuclear translocation of Stat6 induced by IL-4 stimulation, suggesting that this treatment impairs the IL-4/Stat6 signaling pathway in BMDCs. Unexpectedly, Glyteer treatment did not potently upregulate the expression of Cyp1a1, a specific Ahr-responsive gene, suggesting that its inhibitory machinery for Ccl17 and Ccl22 expression is likely to operate in an Ahr-independent manner. These findings indicate that Glyteer may exhibit therapeutic potential for AD by downregulating the CCL17 and CCL22 production from DCs in a Th2-deviated microenvironment.
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