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Allergy

Pollutants drive atopic dermatitis

Nature Reviews Immunology volume 17, page 1 (2017)Cite this article

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Initial experiments showed that AhR-CA mice (which express a constitutively active form of AhR in keratinocytes) develop an inflammatory skin disease resembling atopic dermatitis and characterized by infiltration of allergic-type immune cells, pruritus (itching) and barrier dysfunction in the skin. Pro-inflammatory and type 2 cytokines, including thymic stromal lymphopoietin (TSLP), interleukin-18 (IL-18), IL-33, IL-4 and IL-13, were also upregulated in the skin of AhR-CA mice, with ChIP-seq analyses in primary keratinocytes showing that the AhR-CA construct binds to the promoter and intronic regions of Tslp and Il33, respectively. Both TSLP and IL-33 have been shown to induce dermatitis when overexpressed in mice. Therefore, these findings support the idea that AhR-mediated changes in gene expression induce the development of dermatitis in AhR-CA mice.

In a similar manner to patients with atopic dermatitis, AhR-CA mice also showed enhanced allergic-type sensitization against cutaneously applied antigens. Compared with wild-type mice, AhR-CA mice developed increased T helper 2 (TH2) cell responses in draining lymph nodes following cutaneous application of ovalbumin (OVA) and showed an asthma-like response to subsequent intranasal challenge with OVA. The authors found that scratching behaviours contributed to antigen penetration and percutaneous sensitization; AhR-CA mice that had their nails clipped showed improved barrier function, had lower numbers of OVA-bearing cells in draining lymph nodes and fewer CD4+ T cells in the skin.

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References

  1. Hidaka, T. et al. The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin. Nat. Immunol. http://dx.doi.org/10.1038/ni.3614 (2016)

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Authors
  1. Yvonne Bordon
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Bordon, Y. Pollutants drive atopic dermatitis. Nat Rev Immunol 17, 1 (2017). https://doi.org/10.1038/nri.2016.141

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  • DOI: https://doi.org/10.1038/nri.2016.141

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