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IL-12 protects from psoriasiform skin inflammation

Author

Listed:
  • Paulina Kulig

    (Institute of Experimental Immunology, University of Zurich)

  • Stephanie Musiol

    (Experimental Immunology Unit, Centre of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Centre Munich)

  • Sandra Nicole Freiberger

    (University Hospital Zurich)

  • Bettina Schreiner

    (Institute of Experimental Immunology, University of Zurich)

  • Gabor Gyülveszi

    (Institute for Research in Biomedicine, Cellular Immunology)

  • Giancarlo Russo

    (Functional Genomics Center Zurich, University of Zurich and ETH Zurich)

  • Stanislav Pantelyushin

    (Institute of Experimental Immunology, University of Zurich)

  • Kenji Kishihara

    (Faculty of Pharmaceutical Sciences, Nagasaki International University)

  • Francesca Alessandrini

    (Experimental Immunology Unit, Centre of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Centre Munich)

  • Thomas Kündig

    (University Hospital Zurich)

  • Federica Sallusto

    (Institute for Research in Biomedicine, Cellular Immunology)

  • Günther F.L. Hofbauer

    (University Hospital Zurich)

  • Stefan Haak

    (Experimental Immunology Unit, Centre of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Centre Munich)

  • Burkhard Becher

    (Institute of Experimental Immunology, University of Zurich)

Abstract

Neutralization of the common p40-subunit of IL-12/23 in psoriasis patients has led to a breakthrough in the management of moderate to severe disease. Aside from neutralizing IL-23, which is thought to be responsible for the curative effect, anti-p40 therapy also interferes with IL-12 signalling and type 1 immunity. Here we dissect the individual contribution of these two cytokines to the formation of psoriatic lesions and understand the effect of therapeutic co-targeting of IL-12 and IL-23 in psoriasis. Using a preclinical model for psoriatic plaque formation we show that IL-12, in contrast to IL-23, has a regulatory function by restraining the invasion of an IL-17-committed γδT (γδT17) cell subset. We discover that IL-12 receptor signalling in keratinocytes initiates a protective transcriptional programme that limits skin inflammation, suggesting that collateral targeting of IL-12 by anti-p40 monoclonal antibodies is counterproductive in the therapy of psoriasis.

Suggested Citation

  • Paulina Kulig & Stephanie Musiol & Sandra Nicole Freiberger & Bettina Schreiner & Gabor Gyülveszi & Giancarlo Russo & Stanislav Pantelyushin & Kenji Kishihara & Francesca Alessandrini & Thomas Kündig , 2016. "IL-12 protects from psoriasiform skin inflammation," Nature Communications, Nature, vol. 7(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13466
    DOI: 10.1038/ncomms13466
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