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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\u2010tumor necrosis factor\u2010\u03b1 therapy, when compared with T\u2010cell depletion therapies, should provoke us to critically re\u2010evaluate the current hypothesis for psoriasis pathogenesis. Recently made discoveries regarding other T\u2010cell populations such as Th17 and regulatory T cells, dendritic cells, macrophages, the keratinocyte signal transduction and novel cytokines including interleukin (IL)\u201022, IL\u201023 and IL\u201020, let us postulate that the pathogenesis of psoriasis consists of distinct subsequent stages, in each of them different cell types playing a dominant role. 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