Immune-mediated cytotoxic destruction of epidermal cells is the central mechanism of several inflammatory skin conditions, including vitiligo, alopecia areata and toxic epidermal necrolysis. In these conditions, an IFN-γ dominant cytotoxic response is responsible for the destruction of melanocytes, hair follicles or keratinocytes, respectively. The limited therapeutic efficacy of conventional immunosuppressants and biologicals is striking in these diseases. Previously, our research group conducted the first ever trial of IL-17 inhibition (secukinumab) in vitiligo, which clearly demonstrated that IL-17 inhibition was not an effective treatment strategy. Follow-up experiments also demonstrated that increased numbers of IFN-γ+IL-17+ Th17 cells (Th17.1) could explain increased activation of the Th17 pathway in earlier studies. Targeting the plasticity of the Th17 pathway is therefore a potential new treatment strategy in the long term. In this project, we will study whether a combination treatment that inhibits the cytokine panel responsible for Th17 plasticity is an efficient and feasible strategy to stop the autoimmune-mediated destruction of epidermal cells.