Abstract
Recent studies have provided new insights into the molecular mechanisms involved in the pathogenesis of psoriasis. Patients may inherit a predisposition to psoriasis, although the disease is expressed only after being triggered by certain environmental or antigenic factors. There is considerable genetic heterogeneity in psoriasis and several genetic loci associated with the occurrence of the disease have been identified. Although the underlying abnormality in psoriasis has not been definitively identified, recent evidence suggests that activated T lymphocytes play an important role in the pathogenesis of the disease. The activation of T lymphocytes can be mediated through antigen‐presenting cells or through autoimmunity, and is influenced by cytokines. Recently developed animal models and in vitro studies of psoriasis have provided new evidence for the role of pathogenic lymphocytes in the initiation of the disease process. Further research will help to identify the susceptibility genes involved in psoriasis and provide a more complete understanding of the immunological basis of the disease. This should lead to the development of targeted therapies with improved efficacy and tolerability compared with some currently available treatments.