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Lysosome Alterations in the Human Epithelial Cell Line HaCaT and Skin Specimens: Relevance to Psoriasis

The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis

Laboratory of Experimental Immunology, IDI-IRCCS, via Monti di Creta, 104, 00167 Rome, Italy
Section of Dermatology, Department of Medicine, University of Verona, P.zza Stefani, 1, 37126 Verona, Italy
Department of Medicine, Radboud University Medical Center, 6525 HP Nijmegen, The Netherlands
Department of Medicine, School of Medicine, University of Colorado, Denver, Anschutz Campus, Aurora, CO 80045, USA
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(13), 3318;
Received: 20 May 2019 / Revised: 26 June 2019 / Accepted: 4 July 2019 / Published: 5 July 2019
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
Psoriasis is an immune-mediated inflammatory skin disease that involves mainly T helper (Th)17, Th1 and Th22 lymphocytes, which cause hyper-proliferation of the epidermis with aberrant differentiation of keratinocytes, and local production of chemokines and cytokines. These fuel a self-amplifying loop where these products act on T cells to perpetuate cutaneous inflammatory processes. Among the various inflammatory mediators involved, interleukin (IL)-36 cytokines are important for the recruitment and activation of neutrophils and Th17 cells in psoriatic skin. In particular, IL-36s induce chemokines and cytokines interfere with differentiation/cornification programs in the epidermis, as well as promote pathological angiogenesis and endothelial cell activation. IL-36 cytokines belong to the IL-1 family, and comprise IL-36α, IL-36β, and IL-36γ agonists as well as IL-36 receptor antagonist and IL-38 antagonists. IL-36 cytokines are up-regulated in psoriatic epidermis, and their expression is strongly induced by TNF-α and IL-17. Contrarily, IL-38 antagonist is downregulated, and its impaired expression may be relevant to the dysregulated inflammatory processes induced by IL-36. Here, we discuss on the pathogenic mechanisms leading to the altered balance of IL-36 agonists/antagonists and the significance of this dysregulation in psoriasis. Collection of the information will provide a theoretical basis for the development of novel therapeutic strategies based on IL-36 agonist/antagonist manipulation in psoriasis. View Full-Text
Keywords: psoriasis; IL-36; IL-38; IL-17; skin inflammation psoriasis; IL-36; IL-38; IL-17; skin inflammation
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MDPI and ACS Style

Madonna, S.; Girolomoni, G.; Dinarello, C.A.; Albanesi, C. The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis. Int. J. Mol. Sci. 2019, 20, 3318.

AMA Style

Madonna S, Girolomoni G, Dinarello CA, Albanesi C. The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis. International Journal of Molecular Sciences. 2019; 20(13):3318.

Chicago/Turabian Style

Madonna, Stefania, Giampiero Girolomoni, Charles A. Dinarello, and Cristina Albanesi. 2019. "The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis" International Journal of Molecular Sciences 20, no. 13: 3318.

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