There has been a recent explosion in knowledge regarding the central role of the immune system in the pathogenesis of psoriasis. Originally felt to be primarily a disorder of keratinocyte hyperproliferation, it has recently been classified as a T cell-mediated, autoimmune disease. Type 1 cytokines released predominantly from activated T lymphocytes are now considered to cause the psoriatic phenotype, including the epidermal and vascular changes. Armed with this new knowledge, pharmaceutical and biotechnology companies have developed more specific, immunologically directed interventions. These newer agents aim to be both more effective in clearing a condition that is associated with much morbidity and to be more selective, resulting in fewer toxic side effects than current therapies. This article gives an overview of the newer immunotherapeutic approaches from the points of view of safety, efficacy and mechanisms of action. The review also outlines the steps involved in the immune response leading to psoriasis and considers how each step could offer a target for therapeutic intervention. Infliximab, etanercept, alefacept and efalizumab are considered in detail.
