The presence of polymorphonuclear neutrophils (PMN) is a constant feature of Psoriatic epidermis. The reasons for this migratory activity are not clear and may be related to the presence of chemotaxigens or chemoattractants (circulating immune complexes, complement split products, or arachidonic acid metabolites) in serum and/or epidermis. On the other hand, functional abnormalities of psoriatic PMN may play a significant role as well. PMN chemotaxis, e.g., against increased chemoattractants has been found to be significantly increased in psoriasis. On the basis of these findings it may be suggested, that potent chemotaxigens or chemoattractants together with hyperactive PMN by the liberation of lysosomal enzymes cause a self-augmented increase of chemotactic factors. Recent experiments using PMN and sera from patients with psoriasis appear to support this concept. Modulating influences of immunoglobulins, specifically immunoglobulin A have recently been discovered. In chronic stationary psoriasis chemotactic activity of PMN is strongly inhibited which appears to be due to increased levels of IgA. Further, in inflammatory dermatoses with predominantly neutrophils similar IgA-related chemotaxis depression has been found. This appears to be a newly found modulation of PMN-dependent inflammatory reactions in the skin.