Psoriasis is a chronic
skin disease that affects about 1.5% of the Caucasian population and is characterized by typical macroscopic and microscopic skin alterations. Psoriatic lesions are sharply demarcated, red and slightly raised lesions with
silver-whitish scales. The microscopic alterations of psoriatic plaques include an infiltration of immune cells in the dermis and epidermis, a dilatation and an increase in the number of blood vessels in the upper dermis, and a massively thickened epidermis with atypical keratinocyte differentiation. It is considered a fact that the immune system plays an important role in the pathogenesis of
psoriasis. Since the early 1990s, it has been assumed that T1 cells play the dominant role in the initiation and maintenance of
psoriasis. However, the profound success of anti-
tumor necrosis factor-alpha therapy, when compared with T-cell depletion
therapies, should provoke us to critically re-evaluate the current hypothesis for
psoriasis pathogenesis. Recently made discoveries regarding other T-cell populations such as Th17 and regulatory T cells, dendritic cells, macrophages, the keratinocyte signal transduction and novel
cytokines including
interleukin (IL)-22,
IL-23 and
IL-20, let us postulate that the pathogenesis of
psoriasis consists of distinct subsequent stages, in each of them different cell types playing a dominant role. Our model helps to explain the varied effectiveness of the currently tested immune modulating
therapies and may enable the prediction of the success of future
therapies.