IL-12 protects from psoriasiform skin inflammation

Paulina Kulig; Stephanie Musiol; Sandra Nicole Freiberger; Bettina Schreiner; Gabor Gyülveszi; Giancarlo Russo; Stanislav Pantelyushin; Kenji Kishihara; Francesca Alessandrini; Thomas Kündig; Federica Sallusto; Günther F.L. Hofbauer; Stefan Haak; Burkhard Becher

doi:10.1038/ncomms13466

Nature Communications (Nov 2016)

IL-12 protects from psoriasiform skin inflammation

Paulina Kulig,
Stephanie Musiol,
Sandra Nicole Freiberger,
Bettina Schreiner,
Gabor Gyülveszi,
Giancarlo Russo,
Stanislav Pantelyushin,
Kenji Kishihara,
Francesca Alessandrini,
Thomas Kündig,
Federica Sallusto,
Günther F.L. Hofbauer,
Stefan Haak,
Burkhard Becher

Affiliations

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: Department of Dermatology, 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: Department of Immunology, 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: Department of Dermatology, University Hospital Zurich
Federica Sallusto: Institute for Research in Biomedicine, Cellular Immunology
Günther F.L. Hofbauer: Department of Dermatology, 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

DOI: https://doi.org/10.1038/ncomms13466
Journal volume & issue: Vol. 7, no. 1
pp. 1 – 14

Abstract

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IL-12 and IL-23 share the common p40 subunit yet have distinct immunological functions with IL-12 typically contributing to Th1 responses and IL-23 to Th17 responses. Here the authors show that current p40 based therapies for psoriasis are counterproductive owing to an IFN-γ-independent tissue protective function of IL-12 in skin.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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