Pemphigus vulgaris (PV) is an autoimmune blistering disease, specifically targeting the skin and mucous membranes. IgG-autoantibodies against desmogleins 3 (dsg3) and/or dsg1 are characteristics of PV. Their influence against the named autoantigens in the skin cause the adhesions between keratinocytes to disrupt, resulting in intraepidermal blistering, known as acantholysis, which can also be observed in mucosal areas. This can be potentially life-threatening to patients, like other autoimmune skin blistering diseases. Current options of therapy involve high dose, systemic prednisolone, a glucocorticosteroid (for general immunosuppression), immunoapheresis of circulating antibodies, and intravenous administration of immunoglobulins, including the anti-CD20-antibody rituximab.Immun osuppression is the main effect of these approaches, resulting in a significant numbeof side-effects.I will be testing substances influencing protein biosynthesis in the human skin organ culture model (HSOC) for pemphigus vulgaris. The aim is to clarify if these substances reduce the amount of split formation in the HSOC, so that they could potentially function as a therapeutic option in the future to stop new blisters from forming in patients suffering from pemphigus vulgaris.