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

Abstract	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.
Authors	Takanori Hidaka, Eisaku Ogawa, Eri H Kobayashi, Takafumi Suzuki, Ryo Funayama, Takeshi Nagashima, Taku Fujimura, Setsuya Aiba, Keiko Nakayama, Ryuhei Okuyama, Masayuki Yamamoto
Journal	Nature immunology (Nat Immunol) Vol. 18 Issue 1 Pg. 64-73 (01 2017) ISSN: 1529-2916 [Electronic] United States
PMID	27869817 (Publication Type: Journal Article)
Chemical References	AHR protein, human ARTN protein, human Ahr protein, mouse Air Pollutants Basic Helix-Loop-Helix Transcription Factors Keratin-15 Krt15 protein, mouse Nerve Tissue Proteins Receptors, Aryl Hydrocarbon Ephb2 protein, mouse Receptor, EphB2
Topics	Air Pollutants (adverse effects) Animals Animals, Newborn Axon Guidance (genetics) Basic Helix-Loop-Helix Transcription Factors (genetics, metabolism) Cells, Cultured Dermatitis, Atopic (immunology) Epidermis (innervation, pathology) Gene Expression Regulation Humans Keratin-15 (genetics, metabolism) Keratinocytes (physiology) Mice Mice, Inbred C57BL Mice, Knockout Nerve Tissue Proteins (genetics, metabolism) Pruritus (immunology) Receptor, EphB2 (genetics, metabolism) Receptors, Aryl Hydrocarbon (genetics, metabolism)

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