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

Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis

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

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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Crossref · 10.3390/ijms20215424

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  • Ahr null mice have increased susceptibility to psoriasis, experimental colitis, colorectal cancer, and infections by Citrobacter rodentium and Toxoplasma gondii.

    “Subsequent examination of this mouse has revealed significant defects in resident immune cell populations in the gut, lung, and skin as well as increased susceptibility to certain diseases including psoriasis, experiment colitis and colorectal cancer, and infections of microorganisms like Citrobacter rodentium and Toxoplasma gondii (Díaz-Díaz et al., 2016; Furue et al., 2019; H. R. Kim et al., 202”

    From Rodent Genetic Models of Ah Receptor Signaling (2021) · cites this paper as Furue et al., 2019

    Section 4, “AHR and Immune Modulation” (page unavailable), says C. rodentium-induced colitis becomes life-threatening in Ahr-deficient mice. Section 6, “AHR and Psoriasis” (page unavailable), reports exacerbated inflammation in an imiquimod-induced psoriasis model. The copy does not establish increased susceptibility to experimental colitis as a separate condition, colorectal cancer, or Toxoplasma gondii infection. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Ahr null mice have significant defects in resident immune cell populations in the gut, lung, and skin.

    “Subsequent examination of this mouse has revealed significant defects in resident immune cell populations in the gut, lung, and skin as well as increased susceptibility to certain diseases including psoriasis, experiment colitis and colorectal cancer, and infections of microorganisms like Citrobacter rodentium and Toxoplasma gondii (Díaz-Díaz et al., 2016; Furue et al., 2019; H. R. Kim et al., 202”

    From Rodent Genetic Models of Ah Receptor Signaling (2021) · cites this paper as Furue et al., 2019

    Section 4 (AHR and Immune Modulation; page unavailable) reports losses of intestinal ILC3 cells and decreases in specific gut Treg subpopulations with Ahr deficiency. Section 6 (AHR and Psoriasis; page unavailable) describes altered skin inflammation and IL-22 production, but does not establish defects in skin-resident immune cell populations; the searched passages also do not establish defects in lung-resident populations. The claim extends the documented gut findings to the lung and skin. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • AHR is a ligand-dependent transcription factor activated by multiple compounds that can induce either epidermal differentiation or oxidative stress.

    “AHR, a ligand-dependent transcription factor, is activated by multiple compounds that can induce either epidermal differentiation or oxidative stress (43, 44).”

    From Particulate matter causes skin barrier dysfunction. (2021) · cites this paper as [44]

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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
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2019-10-31
Volume
20
Issue
21
Pages
5424
ISSN
1422-0067 (ISSN-L)
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 · 2018: 2
FWCI
3.68
Type
journal article
Language
en
Open access
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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