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
Patruno, Cataldo;
2018-01-01
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
