Psoriasis is a multigenic disease with a number of susceptibility loci on different chromosomes predisposing to the disease, which is in turn triggered by environmental factors. The pathogenesis of psoriasis is characterized by 2 main components, the dysfunctions of the immune system and the alteration of keratinocyte homeostasis. While the Th1 T cell response has long been considered the sole immune agent in the pathomechanisms of psoriasis, recently, the role of IL-23-driven Th17 has been shown to be predominant. Subsequently, only effector memory T cells expressing alpha1beta1 integrin migrate into the epidermis, and psoriasis development is inhibited by blocking this integrin. Psoriatic epidermis contains high amounts of antimicrobial peptides, which have been shown to be a key mediator of plasmocytoid dendritic cell activation in psoriasis. The keratinocyte component has recently regained the central stage, as the abrogation of JunB/activator protein 1 in mouse keratinocytes induces development of psoriasiform lesions in T cell deficient mice. Moreover, inhibition of nerve growth factor and its receptor in keratinocytes strikingly improves psoriatic lesions.