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Nat Immunol. 2017 Jan;18(1):64-73. doi: 10.1038/ni.3614. Epub 2016 Nov 21.

The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin.

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Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Department of Dermatology, Shinshu University School of Medicine, Matsumoto, Japan.
Division of Cell Proliferation, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tohoku Medical-Megabank Organization, Sendai, Japan.


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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