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Review

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

1
Laboratory of Experimental Immunology, IDI-IRCCS, via Monti di Creta, 104, 00167 Rome, Italy
2
Section of Dermatology, Department of Medicine, University of Verona, P.zza Stefani, 1, 37126 Verona, Italy
3
Department of Medicine, Radboud University Medical Center, 6525 HP Nijmegen, The Netherlands
4
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; https://doi.org/10.3390/ijms20133318
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. https://doi.org/10.3390/ijms20133318

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. https://doi.org/10.3390/ijms20133318

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. https://doi.org/10.3390/ijms20133318

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