Psoriasis affects approximately 2% of the population in Western countries. Although clinically rather monomorphic, the disease presents with a number of phenotypically distinct and heterogeneous subgroups showing differences in their pathogenetic pathways. Patients with type I (early onset) psoriasis demonstrate inflammatory lesions with epidermal hyperproliferation and the presence of activated T cells as well as intraepidermal polymorphs as principal features. In contrast to pustular types of psoriasis, these patients show genetic susceptibility and strong association with MHC class I and class-I haplotypes. There is evidence for a T-cell-mediated pathomechanism leading to a large spectrum of regulatory mediators including cytokines and growth factors as well as lipid mediators which are abnormally expressed. Pathogenetically psoriasis shows features in common with chronic relapsing T-cell-mediated diseases including Crohn’s disease, rheumatoid arthritis and others.