Role of Aryl Hydrocarbon Receptor Activation and Autophagy in Psoriasis-Related Inflammation
Open accessAbstract
Aryl hydrocarbon receptor (AhR) and autophagy reportedly regulate immune responses in the skin. This study explored the effects of AhR activation on autophagy in human keratinocytes, and the relevance of AhR and autophagy in psoriasis pathogenesis. AhR activation by 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) repressed autophagy, while autophagy inhibition induced AhR activation in HaCaT cells and normal human epidermal keratinocytes (NHEKs). A particularly strong interaction between AhR and autophagy was observed in proinflammatory cytokines-stimulated keratinocytes, an in vitro model of psoriasis. In skin biopsies from psoriasis patients, a similar impact of AhR on autophagy and inflammation was observed. AhR inhibition blocked TCDD- and chloroquine-induced p65NF-κB and p38MAPK phosphorylation in proinflammatory cytokines-stimulated HaCaT cells. Moreover, higher expression of AhR and CYP1A1, and lower expression of LC3, were detected in psoriatic skin tissues, compared to the controls. These data demonstrated that AhR modulated autophagy leads to skin inflammation in human keratinocytes via the p65NF-κB/p38MAPK signaling pathways, suggesting that AhR signaling and autophagy might be involved in the pathogenesis of chronic inflammatory disorders such as psoriasis.
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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 H. R. Kim et al., 2020
The Introduction (page unavailable) says AhR affects the maturation and function of skin Langerhans cells, and the References list a study of impaired Langerhans-cell maturation in AhR-null mice. That provides limited support for a skin immune-cell defect, but the cited paper does not report defects in resident immune-cell populations across the gut, lung, and skin. (LLM, conf=0.78)
Experimental — accuracy not yet measuredAhr 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 H. R. Kim et al., 2020
The Results (§2.7) examine human psoriasis skin biopsies, and the Discussion (§3) discusses AhR activation in keratinocytes and psoriatic inflammation. Searches for AhR-null mice, susceptibility, colitis, colorectal cancer, Citrobacter rodentium, and Toxoplasma gondii found no passage reporting the claimed disease or infection susceptibility in AhR-null mice. (LLM, conf=0.75)
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- Authors
- Kim, H. R., Kang, S. Y., Kim, H. O., Park, C. W., & Chung, B. Y.
- Affiliations
- Hallym University Kangnam Sacred Heart Hospital (KR)
- Corresponding author
- Chung, Bo Young
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-03-22
- Volume
- 21
- Issue
- 6
- Pages
- 2195
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7139675
- OpenAlex
- W3012657936
- Cited by
- 52
- References
- 45
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 12 · 2023: 11 · 2022: 8 · 2021: 8 · 2020: 2
- FWCI
- 2.54
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation of Korea (NRF) (2018R1C1B6007998)
- Hallym University Research Fund (HURF-2019-72)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- aryl hydrocarbon receptor, autophagy, psoriasis, keratinocytes, skin inflammation, 2,3,7,8-tetrachlorodibenzo-p-dioxin, NF-κB signaling, p38 MAPK signaling, CYP1A1, LC3, inflammatory cytokines, chloroquine
- MeSH terms
- Animals, Autophagy, Cell Line, Cells, Cultured, Humans, Inflammation, Psoriasis, Skin, Keratinocytes, Receptors, Aryl Hydrocarbon, Basic Helix-Loop-Helix Transcription Factors, Basic Helix-Loop-Helix Proteins
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