Psoriasis is considered to be a genetically programmed disease of dysregulated inflammation, which is driven and maintained by multiple components of the immune system. The pathologic collaboration between innate immunity (mediated by antigen-presenting cells and natural killer T lymphocytes) and acquired immunity (mediated by T lymphocytes) results in the production of cytokines, chemokines, and growth factors that contribute to the inflammatory infiltrate seen in psoriatic plaques. This overview of the pathophysiology of psoriasis describes these events, and recent developments that have contributed to our understanding of the role of immune function in psoriasis. These developments include the creation of useful animal models and identification of new receptors and lymphocyte subtypes that may participate in the development of this chronic disease.