Evidence for a key role of T cells in the pathogenesis of psoriasis has come from both experimental and clinical data. Initially, generalized immunosuppressants, intended for use in transplant settings, were found to improve clinical signs and symptoms of psoriasis. Their efficacy attracted attention to the activated T cells that are a major component of the inflammatory infiltrate of psoriatic lesions. Further research determined that T cells from patients with psoriasis could transmit disease in animal models. These findings laid the groundwork for characterizing the pathogenesis of psoriasis as immune mediated with skin‐directed T cells playing a central role. Once these pathogenic T cells have entered the skin, they become activated and release cytokines and chemokines to attract other immune cells to perpetuate the inflammatory cascade. As the role of the T cell in psoriasis has evolved and understanding of immunopathology has increased, a multitude of biologic targets have been revealed. Newer strategies for the treatment of psoriasis have therefore focused on modifying T cells in this disease through direct elimination of activated T cells, inhibition of T‐cell activation, or inhibition of cytokine secretion or activity. The mechanisms by which these new biologic agents act on psoriasis will affect their profile of efficacy and safety. Important selection criteria for optimal antipsoriatic therapies include long‐term safety and tolerability, ability to produce long‐lasting remissions, and convenient dosing regimens.