In this study, we investigated the role of IL-26 in allergic contact dermatitis (ACD), highlighting its contribute in the cytotoxic mechanism responsible of the tissue injury. IL-26 is a signature Th17 cytokine, and immune cells are its predominant sources. Recently, it has shown that Th17 cell-derived-IL-26 functions like an antimicrobial peptide. Here, we hypothesized that IL-26 could be involved in cytotoxicity mechanism, that underlies ACD. Indeed, we have attributed a role to IL-26 in this context, through PBMC cytotoxicity assays versus Hacat. In order to demonstrate that IL-26 was effectively involved in this activity, we performed the assay using transfected ACD PBMCs by siRNA for IL-26. Indeed, we demonstrated that these cells were less able to kill keratinocytes compared to ACD PBMC (p<0.01). In conclusion, our findings support the idea that this emergent cytokine, IL-26, is implicated in the killing mechanisms of KC observed during ACD. This article is protected by copyright. All rights reserved.
IL-26 in allergic contact dermatitis: resource in a state of readiness / Caiazzo, Giuseppina; Caprio, Roberta Di; Lembo, Serena; Raimondo, Annunziata; Scala, Emanuele; Patruno, Cataldo; Balato, Anna. - In: EXPERIMENTAL DERMATOLOGY. - ISSN 0906-6705. - (2018). [10.1111/exd.13521]
IL-26 in allergic contact dermatitis: resource in a state of readiness
Caiazzo, Giuseppina;Caprio, Roberta Di;Lembo, Serena;Raimondo, Annunziata;Scala, Emanuele;Patruno, Cataldo;Balato, Anna
2018
Abstract
In this study, we investigated the role of IL-26 in allergic contact dermatitis (ACD), highlighting its contribute in the cytotoxic mechanism responsible of the tissue injury. IL-26 is a signature Th17 cytokine, and immune cells are its predominant sources. Recently, it has shown that Th17 cell-derived-IL-26 functions like an antimicrobial peptide. Here, we hypothesized that IL-26 could be involved in cytotoxicity mechanism, that underlies ACD. Indeed, we have attributed a role to IL-26 in this context, through PBMC cytotoxicity assays versus Hacat. In order to demonstrate that IL-26 was effectively involved in this activity, we performed the assay using transfected ACD PBMCs by siRNA for IL-26. Indeed, we demonstrated that these cells were less able to kill keratinocytes compared to ACD PBMC (p<0.01). In conclusion, our findings support the idea that this emergent cytokine, IL-26, is implicated in the killing mechanisms of KC observed during ACD. This article is protected by copyright. All rights reserved.File | Dimensione | Formato | |
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