Psoriasis vulgaris, roughly translated as vulgar scaling, is a complex inflammatory skin disease that affects approximately 2% of the Western population. It presents with a characteristic type of skin lesions that appear as sharply demarcated reddish plaques of variant size covered with intensive silvery scaling. In a significant proportion of patients (>10%) psoriasis also involves the joints, sometimes leading to severe arthritis. Psoriasis has been recognized since ancient times, but it was only after 1800 that it was clearly distinguished from leprosy. Since then its pathophysiology has been an intellectual challenge and has stimulated a large variety of experimental investigations. All attempts to explain the aetiology of psoriasis, however, faced a major problem: they had to integrate into a conclusive pathophysiological concept a particular combination of seemingly unrelated features that are unique for psoriasis: keratinocytes in psoriatic skin lesions show a reversible state of excessive hyperproliferation thus giving rise to increased epidermal turnover and scaling; neutrophilic granulocytes accumulate in the upper epidermal layers where they form small intra-epithelial abscesses; increased numbers of activated mast cells are observed in lesional dermis; skin lesions harbour a dense lesional infiltrate of mononuclear cells with numerous activated T lymphocytes that exocytose from dermis into epidermis; and psoriasis manifestations are often provoked by throat infections with group A beta-haemolytic streptococci. These changes are manifested against a strong yet polygenetic hereditary background: besides several gene loci inconsistently associated with psoriasis, an immunogenetic predisposition is most evident. Several HLA-molecules of the class I (Cw6, B13, Bw57) and class II locus (DR 7) were observed to confer a particular risk for psoriasis [1]. This HLA-association was recognized in 1972 and indicated for the first time that psoriasis was not due to formerly suspected inhereted defects in keratinocyte growth regulation, neutrophil function, mediators of inflammation, etc., but rather involved immunological mechanisms. Further observations soon corroborated this supposition. Infiltration of activated T lymphocytes was found to precede the eruption of psoriatic skin lesions, and a decrease in the density of infiltrating T-cells is a sensitive indicator for disease resolution [2]. In the dermis, the majority of infiltrating T-cells are CD4 + , while T-cells infiltrating into the dermis predominantly belong to the CD8 + subset. Many of the activated T-cells observed in psoriatic dermis are closely associated with dendritic cells expressing MHC class II molecules [3]. Furthermore, psoriasis exacerbations can be triggered by systemic application of the T-cell growth factor IL-2, or of IFN-a or IFN-b [4‐6]. The disease can be transferred by, or resolves after, bone marrow transplantation and some immunosuppressive treatments are highly effective. In particular, the therapeutic efficacy of T-cell selective immunosuppressive regimens such as ciclosporin, monoclonal CD4 antibodies or a lymphocyte-selective toxin composed of IL-2 and fragments of diphtheria toxin has demonstrated that the formation of psoriatic skin lesions crucially depends on activated T lymphocytes [7‐9]. Based on these findings, psoriasis has been regarded as a disease of abnormal keratinocyte proliferation that is induced by T lymphocytes [2]. This conclusion raised several questions essential for a further understanding of psoriasis: how can Tcells transmit a disease that on first sight has so little to do with an immunologically mediated disorder, and how do these T-cells