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Kulig, P.* ; Musiol, S. ; Freiberger, S.N.* ; Schreiner, B.* ; Gyulveszi, G.* ; Russo, G.* ; Pantelyushin, S.* ; Kishihara, K.* ; Alessandrini, F. ; Kundig, T.* ; Sallusto, F.* ; Hofbauer, G.F.L.* ; Haak, S. ; Becher, B.*

IL-12 protects from psoriasiform skin inflammation.

Nat. Commun. 7:13466 (2016)
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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 gdT (gdT17) 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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Delta T-cells; Interleukin-12/23 Monoclonal-antibody; Chronic Plaque Psoriasis; Necrosis-factor-alpha; Gamma-delta; Interferon-gamma; Epidermal-keratinocytes; Increased Expression; Gene-expression; Cutting Edge
Sprache englisch
Veröffentlichungsjahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 7, Heft: , Seiten: , Artikelnummer: 13466 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Allergy Research (IAF)
POF Topic(s) 30202 - Environmental Health
Forschungsfeld(er) Allergy
PSP-Element(e) G-505400-004
DOI 10.1038/ncomms13466
WOS ID WOS:000389038800001
Erfassungsdatum 2016-12-31
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