| Abstrakt: |
Psoriasis is a relatively common, chronic skin disease affecting 1-2% of the population in the developed countries. It is an inflammatory, autoimmune skin disorder characterised by an accelerated rate of epidermal proliferation and disordered differentiation. Since our last review in 1999, considerable progress has been made in understanding the immunopathogenesis of this disease, and new drugs have become available for its treatment. Recent clinical trials showed the efficacy of novel biotechnology approaches, such as blocking tumour necrosis factor-alpha or T-cell-mediated immune response by the anti-CD2, anti-CD11a, anti-B7, anti-CD4 or anti-CD25 approaches. Agents which block type 1 cytokines or skew immune reactions into type 2 are other promising approaches. Other possible targets are chemokines and their receptors, the cytokines and receptors involved in T cell trafficking into the skin, and peroxisome proliferator-activated receptors. Relatively little development is reported of the drugs targeting the keratinocyte or the classical antipsoriatic compounds which include glucocorticoids, vitamin D derivatives and cytostatic agents. |
