ABSTRACT
Psoriasis is known to be an epidermal proliferative disease. This proliferation is due to a shortened cell division cycle time or to a recruitment of normally noncycling cells and is associated with parakeratosis. The fixation of complement on immune-complexes formed in epidermis results in polymorphonuclear attraction and proteolytic enzyme release. Immunological processes could result in epidermal proliferation by modifying the plasma membrane. The viral origin of the T-cell defect is a most attractive hypothesis. No definite proof of a virus in psoriasis is yet available but we have found virus like particules in phyto-hemagglutinin stimulated lymphocyte cultures. The chapter proposes a hypothetical chain leading to psoriasis: genetic and viral factors could induce an immune response imbalance, such dysfunction could explain humoral and cell-mediated immunological abnormalities, epidermal immunological processes could result in keratinocyte membrane dysfunction and membrane abnormalities could result in cyclic nucleotide and prostaglandin imbalance.
