Psoriasis is a chronic inflammatory disorder resulting from a combination of genetic and environmental factors, although the precise causal agents have not yet been identified. The immune system has a major role in the development of psoriasis, and the possibility exists that self antigens, antigens from microbial agents, or microbial superantigens initiate a vigorous immune response. Different subsets of T lymphocytes and dendritic cells, mast cells, and granulocytes participate in the pathogenesis; and several cytokines and chemokines have been identified in tissue lesions. Tumor necrosis factor-alpha, interleukin 17 (IL-17), and IL-23 are key cytokines with important pathogenetic roles in psoriasis. Angiogenesis is a prominent early event in lesional psoriatic skin. Potential targets in the treatment of this disorder include biologic agents aimed at blockade of cytokines, chemokines, and angiogenic factors.