Journal article
IL-12 protects from psoriasiform skin inflammation.
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Kulig P
Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.
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Musiol S
Experimental Immunology Unit, Centre of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Centre Munich, 80802 Munich, Germany.
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Freiberger SN
Department of Dermatology, University Hospital Zurich, 8091 Zurich, Switzerland.
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Schreiner B
Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.
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Gyülveszi G
Institute for Research in Biomedicine, Cellular Immunology, 6500 Bellinzona, Switzerland.
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Russo G
Functional Genomics Center Zurich, University of Zurich and ETH Zurich, 8057 Zurich, Switzerland.
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Pantelyushin S
Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.
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Kishihara K
Department of Immunology, Faculty of Pharmaceutical Sciences, Nagasaki International University, 859-3298 Nagasaki, Japan.
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Alessandrini F
Experimental Immunology Unit, Centre of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Centre Munich, 80802 Munich, Germany.
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Kündig T
Department of Dermatology, University Hospital Zurich, 8091 Zurich, Switzerland.
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Sallusto F
Institute for Research in Biomedicine, Cellular Immunology, 6500 Bellinzona, Switzerland.
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Hofbauer GF
Department of Dermatology, University Hospital Zurich, 8091 Zurich, Switzerland.
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Haak S
Experimental Immunology Unit, Centre of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Centre Munich, 80802 Munich, Germany.
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Becher B
Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.
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Published in:
- Nature communications. - 2016
English
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.
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Language
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Open access status
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gold
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Identifiers
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Persistent URL
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https://sonar.ch/global/documents/184211
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