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TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis

Author

Listed:
  • 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)

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.

Suggested Citation

  • Daniel Sidler & Ping Wu & Rana Herro & Meike Claus & Dennis Wolf & Yuko Kawakami & Toshiaki Kawakami & Linda Burkly & Michael Croft, 2017. "TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis," Nature Communications, Nature, vol. 8(1), pages 1-11, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15395
    DOI: 10.1038/ncomms15395
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