IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment
IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment(170 views visite) Mercurio L, Morelli M, Scarponi C, Eisenmesser EZ, Doti N, Pagnanelli G, Gubinelli E, Mazzanti C, Cavani A, Ruvo M, Dinarello CA, Albanesi C, Madonna S
Cell Death & (ISSN: 2041-4889electronic), 2018 Oct 30; 9(11): 1104-1104.
Keywords Parole chiave: Not available. Non disponibili.
Affiliations Affiliazioni: *** IBB - CNR ***
Laboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy., Section of Dermatology, Department of Medicine, University of Verona, P.zza Stefani, 1, Verona, 37126, Italy., Department of Biochemistry & Molecular Genetics, School of Medicine, University of Colorado Denver, Anschutz Campus, Aurora, 80045, CO, USA., Istituto di Biostrutture e Bioimmagini-CNR and CIRPEB, Via Mezzocannone, 16, Naples, 80134, Italy., 1st Division of Dermatology and CRI-PSO, Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, Rome, 00167, Italy., CRI-PSO Istituto Dermopatico dell'Immacolata, IDI-IRCCS, via Monti di Creta, 104, Rome, 00167, Italy., INMP/NIHMP, via di S.Gallicano, 25, Rome, 00153, 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, USA., Laboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy. s.madonna@idi.it., via di S.Gallicano ,25, Rome, 00153, Italy
References Riferimenti: Not available. Non disponibili.
IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment
IL-36 cytokines, a subgroup of IL-1 family, comprise IL-36alpha, IL-36beta, and IL-36gamma agonists, abundantly expressed in psoriatic skin, and IL-36RA and IL-38 antagonists. In psoriatic skin, IL-36 cytokines interfere with keratinocyte cornification programs and induce the release of antimicrobial peptides and chemokines active on neutrophils and Th17 lymphocytes. To date, the role of IL-38 antagonist in psoriasis remains to be defined. Here, we demonstrate that skin and circulating IL-38 levels are reduced in psoriatic patients and in other skin diseases characterized by neutrophilic infiltrate. In psoriasis, the balance of IL-36gamma agonist/IL-38 antagonist serum levels is in favor of agonists and is closely associated with disease severity. Interestingly, IL-38 is upregulated by anti-IL-17A biological treatment and positively correlates with the therapeutic efficacy of secukinumab in psoriatic patients. The downregulation of IL-38 expression is strictly related to keratinocyte de-differentiation triggered by the inflammatory cytokines IL-36gamma, IL-17, and IL-22. Finally, we demonstrate that administration of recombinant full-length IL-38 counteracts in vitro the biological processes induced by IL-36gamma in human keratinocytes and endothelial cells and attenuates in vivo the severity of the psoriasiform phenotype induced by IMQ in mice. Such effects are achieved by restoring the physiological programs of keratinocyte proliferation and differentiation, and reducing the immune cell infiltrates.
IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment
IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment
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