Cited by 216Dermatology and Skin DiseasesPsoriasis: Treatment and PathogenesisToxic Organic Pollutants Impact

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Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis

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Furue, Masutaka, Hashimoto-Hachiya, Akiko, Tsuji, Gaku·2019·International Journal of Molecular Sciences

DOI 10.3390/ijms20215424PMC PMC6862295

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Abstract

The aryl hydrocarbon receptor (AHR)/AHR-nuclear translocator (ARNT) system is a sensitive sensor for small molecular, xenobiotic chemicals of exogenous and endogenous origin, including dioxins, phytochemicals, microbial bioproducts, and tryptophan photoproducts. AHR/ARNT are abundantly expressed in the skin. Once activated, the AHR/ARNT axis strengthens skin barrier functions and accelerates epidermal terminal differentiation by upregulating filaggrin expression. In addition, AHR activation induces oxidative stress. However, some AHR ligands simultaneously activate the nuclear factor-erythroid 2-related factor-2 (NRF2) transcription factor, which is a master switch of antioxidative enzymes that neutralizes oxidative stress. The immunoregulatory system governing T-helper 17/22 (Th17/22) and T regulatory cells (Treg) is also regulated by the AHR system. Notably, AHR agonists, such as tapinarof, are currently used as therapeutic agents in psoriasis and atopic dermatitis. In this review, we summarize recent topics on AHR related to atopic dermatitis and psoriasis.

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Figure 1 Aryl hydrocarbon receptor (AHR) signal and action points of tapinarof (red words and arrows). AHR is a promiscuous chemical sensor that is activated by various oxidative and antioxidative ligands. Once activated, cytoplasmic AHR translocates into the nucleus where it heterodimerizes with an AHR-nuclear translocator (ARNT) and then induces the transcription of AHR-responsive genes such as cytochrome P450 1A1 (CYP1A1). CYP1A1 degrades AHR ligands. Some ligands such as dioxins are chemically stable and long-lived. Therefore, CYP1A1 generates high amounts of reactive oxygen species (ROS) after sustained efforts to degrade them. Some antioxidative AHR ligands activate nuclear factor-erythroid 2-related factor-2 (NRF2) transcription factor, which upregulates gene expression of various antioxidative enzymes, such as heme oxygenase 1 (HMOX1), NAD(P)H dehydrogenase, and quinone 1 (NQO1), and these antioxidative enzymes neutralize ROS. AHR/ARNT signaling also activates OVO-like 1 (OVOL1) transcription factor and upregulates the expression of filaggrin (FLG) and loricrin (LOR). AHR upregulates the expression of involucrin (IVL) in an OVOL1-independent manner. Therefore, AHR/ARNT signaling accelerates epidermal terminal differentiation and enhances the repair of barrier disruption. Interleukin (IL)-4 and IL-13 activate signal transducer and activator of transcription 6 (STAT6) and inhibit the OVOL1/FLG, OVOL1/LOR, and AHR/IVL axes. However, suitable AHR activation can inhibit the IL-4/IL-13-mediated STAT6 activation and restore the expression of FLG, LOR, and IVL. Regarding immune response, AHR signaling affects T-helper (Th17) differentiation and is essential for IL-22 production. AHR ligation (especially by high concentrations of ligands) induces the differentiation of regulatory cell populations, Treg and Tr1 cells. Tapinarof is an antioxidative AHR ligand and upregulates CYP1A1 expression. Topical tapinarof is efficacious in psoriasis and atopic dermatitis. Current studies demonstrate that tapinarof activates NRF2/antioxidative signaling and reduces oxidative stress. Tapinarof also upregulates FLG and IVL expression. Tapinarof downregulates IL-17A production and increases IL-22 production.CC BY · PubMed Central

Figure 2 Human epidermal keratinocytes are stimulated with 10 ng/mL of IL-4 augments the protein expression of aryl hydrocarbon receptor (AHR) and AHR-nuclear translocator (ARNT) compared with untreated control by Western blot analysis.CC BY · PubMed Central

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Authors: Furue, M., Hashimoto-Hachiya, A., & Tsuji, G.
Affiliations: Kyushu University (JP)
Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan
Corresponding author: Furue, Masutaka
ORCID: Furue, Masutaka
Tsuji, Gaku
Venue: International Journal of Molecular Sciences
Publisher: MDPI AG
Published: 2019-10-31
Volume: 20
Issue: 21
Pages: 5424
ISSN: 1422-0067 (ISSN-L)
DOI: 10.3390/ijms20215424
PMC: PMC6862295
OpenAlex: W2982429666
Cited by: 215
References: 144
Citations by year: 2026: 35 · 2025: 23 · 2024: 42 · 2023: 37 · 2022: 27 · 2021: 27 · 2020: 20 · 2019: 2
FWCI: 3.68
Type: journal article
Language: en
Open access: gold
dx.doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
Locations: International Journal of Molecular Sciences (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: The Ministry of Health, Labour, and Welfare in Japan (H30-Shokuhin-Shitei-005)
The Leading Advanced Projects for Medical Innovation in Japan (The Leading Advanced Projects for Medical Innovation in Japan)
Topics: Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
Keywords: aryl hydrocarbon receptor, ARNT, atopic dermatitis, psoriasis, skin barrier function, filaggrin, oxidative stress, Nrf2, tapinarof, AhR agonists, dioxins, tryptophan metabolites
MeSH terms: Filaggrin Proteins, Animals, Dermatitis, Atopic, T-Lymphocytes, Helper-Inducer, Humans, Psoriasis, Skin, Receptors, Aryl Hydrocarbon, Oxidative Stress, Polymorphism, Single Nucleotide, T-Lymphocytes, Regulatory

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Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis

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