In this study, we investigated the role of IL‐26 in allergic contact dermatitis (ACD), highlighting its’ contribute in the cytotoxic mechanism responsible for 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 vs HaCat. 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 with ACD PBMCs (P < .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.