Psoriasis is a chronic inflammatory skin disorder characterized by accelerated growth and altered differentiation of keratinocytes and angiogenesis with marked ectasia of blood vessels. It develops through interactions between the skin and immune system mediated by T cells, dendritic cells, and inflammatory cytokines. The understanding of the cellular and molecular alterations underlying the disease has advanced, yet the majority of factors leading to the initiation and maintenance of disease remain elusive. Researchers have attempted to reproduce psoriasis in genetically modified and xenotransplantation mouse models to gain insight into its pathogenesis, and they are beginning to use these models to test new therapeutic agents and define mechanisms of action. Every mouse model has strengths and weaknesses, with room for improvement. Still, these models will accelerate knowledge of psoriasis pathogenesis and aid in the development of new therapeutics.