[The role of cytokines for the pathogenesis of psoriasis]

Psoriasis is an inflammatory skin disorder characterized by marked hyperproliferation of keratinocytes in association with vascular expansion, fibroblast activation, leucocyte infiltration, and alterations of eicosanoid metabolism and of cytokine production. However, it is unclear at present whether these changes are the cause or the effect of the significantly increased keratinocyte turnover. More than one mechanism is involved in triggering active psoriasis; genetic predisposition and environmental factors affecting the immune system have a particularly important role. Most of the therapeutic regimens used for the treatment of psoriasis are immunosuppressive. Therefore, it is tempting to speculate that a specific defect of the immune system is the major pathogenic principle in psoriasis. There are several lines of evidence suggesting that changes in cytokine production by keratinocytes and immunocompetent cells in the skin of the patients, particularly of interleukin-6 and TGF alpha, may play an important part in propagation of the inflammatory response in psoriasis. Further studies are required to find how far local T-cell activation is involved as a basic mechanism of initiation and maintenance of the psoriatic inflammatory response. Accordingly, parameters such as the evaluation of cytokine production in vitro and in vivo and the measurement of cellular activation products may be useful in the diagnosis and monitoring of psoriasis.