Psoriasis is a skin disease that originates as a consequence of homeos
tatic disturbances between epithelial cells (keratinocytes), connectiv
e tissue cells (fibrocytes), and inflammatory cells in genetically pre
disposed individuals. It is yet difficult to separate disturbances of
pathogenetic relevance from those which are mere epiphenomena. The var
ious clinical manifestations of psoriasis are demonstrated in this rev
iew and the pathogenesis is displayed on the basis of 2 pathways which
may interact on different levels: (1) Hyperproliferation due to incre
ased production of growth factors which stimulate the epidermis to bec
ome hyperplastic. (2) T-cell activation and subsequent alteration in t
he expression and secretory profile for various cytokines and adhesion
molecules in the skin.