Vitiligo is a common acquired pigmentary disorder, affecting approximately 1% of the world population. It is characterized by the progressive disappearance of melanocytes leading to skin depigmentations. Clinical observations and research findings have provided support that autoimmune responses (mainly T helper 1 response) against melanocyte self-antigens are involved in the pathophysiology of melanocyte destruction. Therefore, a central hypothesis in current vitiligo research is that immune tolerance to melanocyte self-antigens is broken. The aim of this project is to explore the underlying mechanism leading to the disruption of the immune system's normal homeostatic balance (with special attention for dendritic cells and regulatory T cells) and to evaluate therapeutic strategies using an in vivo model for vitiligo. In this experimental setting, vitiligo will be induced actively by skin injury (experimentally Koebner’ phenomenon) to create a standardized, specific, better timed, efficient and very informative model. This model can lend itself for intra-individual, head-to-head comparison of different topical treatments in vitiligo. We believe that this project will provide a broad view on immunosurveillance involved in the immune-mediated destruction of melanocytes. Moreover, it offers an excellent platform for new research opportunities and may contribute to the design of rational strategies to restore tolerance in autoimmune disease.