Journal
NATURE IMMUNOLOGY
Volume 18, Issue 1, Pages 64-73Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3614
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Funding
- Japan Society for the Promotion of Science [KAKENHI 25840001, 15K08257, 25461688, 22118002, 24249015, 26111002]
- Japan Society for the Promotion of Science (AMED-CREST (chronic inflammation))
- Mitsubishi Foundation
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [25461688, 22118002, 26461686, 15K08257] Funding Source: KAKEN
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Atopic dermatitis is increasing worldwide in correlation with air pollution. Various organic components of pollutants activate the transcription factor AhR (aryl hydrocarbon receptor). Through the use of AhR-CA mice, whose keratinocytes express constitutively active AhR and that develop atopic-dermatitis-like phenotypes, we identified Artn as a keratinocyte-specific AhR target gene whose product (the neurotrophic factor artemin) was responsible for epidermal hyper-innervation that led to hypersensitivity to pruritus. The activation of AhR via air pollutants induced expression of artemin, alloknesis, epidermal hyper-innervation and inflammation. AhR activation and ARTN expression were positively correlated in the epidermis of patients with atopic dermatitis. Thus, AhR in keratinocytes senses environmental stimuli and elicits an atopic-dermatitis pathology. We propose a mechanism of air-pollution-induced atopic dermatitis via activation of AhR.
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