Pemphigus vulgaris (PV) is an autoimmune skin blistering disease mediated by autoantibodies against desmoglein-3 and desmoglein-1. By attacking these structures on keratinocyte membranes in the epidermis, acantholysis can occur and flaccid blisters are formed.

In this project, the effects of previously identified substances that have an inhibitory effect on the disintegration of the epidermis shall be tested in NHEK cells and in the human skin organ culture model.