IL-36 signaling in keratinocytes controls early IL-23 production in psoriasis-like dermatitis

Author:

Goldstein Jérémie D1ORCID,Bassoy Esen Y1,Caruso Assunta1,Palomo Jennifer1,Rodriguez Emiliana1,Lemeille Sylvain1ORCID,Gabay Cem12ORCID

Affiliation:

1. Department of Pathology-Immunology, University of Geneva Faculty of Medicine, Geneva, Switzerland

2. Division of Rheumatology, Department of Medicine, University Hospitals of Geneva, Geneva, Switzerland

Abstract

IL-36R signaling plays an important role in the pathogenesis of psoriasis. We ought to assess the specific function of IL-36R in keratinocytes for the pathology of Aldara-induced psoriasis-like dermatitis. Il36rΔK mice presenting deletion of IL-36R in keratinocytes were similarly resistant to Aldara-induced ear inflammation as Il36r−/− mice, but acanthosis was only prevented in Il36r−/− mice. FACS analysis revealed that IL-36R signaling in keratinocytes is mandatory for early neutrophil infiltration in Aldara-treated ears. RNASeq and qRT-PCR experiments demonstrated the crucial role of IL-36R signaling in keratinocytes for induction of IL-23, IL-17, and IL-22 at early time points. Taken together, our results demonstrate that IL-36R signaling in keratinocytes plays a major role in the induction of Aldara-induced psoriasis-like dermatitis by triggering early production of IL-23/IL-17/IL-22 cytokines and neutrophil infiltration.

Funder

Swiss National Science Foundation

Rheumasearch Foundation

Publisher

Life Science Alliance, LLC

Subject

Health, Toxicology and Mutagenesis,Plant Science,Biochemistry, Genetics and Molecular Biology (miscellaneous),Ecology

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