TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis

Daniel Sidler, Ping Wu, Rana Herro, Meike Claus, Dennis Wolf, Yuko Kawakami, Toshiaki Kawakami, Linda Burkly () and Michael Croft ()
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Daniel Sidler: La Jolla Institute for Allergy and Immunology
Ping Wu: Department of Immunology
Rana Herro: La Jolla Institute for Allergy and Immunology
Meike Claus: La Jolla Institute for Allergy and Immunology
Dennis Wolf: Inflammation Biology, La Jolla Institute for Allergy and Immunology
Yuko Kawakami: Cell Biology, La Jolla Institute for Allergy and Immunology
Toshiaki Kawakami: Cell Biology, La Jolla Institute for Allergy and Immunology
Linda Burkly: Department of Immunology
Michael Croft: La Jolla Institute for Allergy and Immunology

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Atopic dermatitis (AD) and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. Here we show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of AD-specific T helper type 2 (Th2) and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in AD, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naive mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in AD and psoriasis.

Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15395

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DOI: 10.1038/ncomms15395

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