Psoriasis is a common autoimmune skin disease characterized by T cell-mediated hyperproliferation of keratinocytes. The cutaneous and systemic overexpression of a variety of proinflammatory cytokines such as TNF-α, IL-1, IL-6, IL-8, IL-15, IL-18, IL-19, IL-20, IL-22, IL-23 and IFN-gamma, has been demonstrated. The cellular composition of the inflammatory infiltrate within the psoriatic plaques, as well as the keratinocytes hyperproliferation, appear to be directed by these cytokines. Here we briefly review the role of cytokines in the pathogenesis of psoriasis. We present evidence that cytokines of type-1 are responsible for the development, maintenance and resolution of psoriatic lesions. In particular, we have focused our attention on recently discovered cytokines. IL-23, but not IL-12, is considered to be a major factor that drives pathogenic Th1 lymphocytes. On the other hand, IL-19, IL-20 and IL-22, cytokines structurally related to IL-10, affect differentiation and migration of human keratinocytes. Importantly, in contrast to IL-10, they show proinflammatory activities and are involved in the pathogenesis of psoriasis. Finally, we discuss the effectiveness of cytokine therapies in psoriasis, in particular anti-TNF therapy.