Pemphigus vulgaris (PV) is an organ-specific autoimmune bullous disease that affects the mucous membranes and/or skin. It is caused by IgG autoantibodies that primarily target desmoglein 3 (dsg3) and/or desmoglein 1 (dsg1). Desmogleins are decisive components of cell adhesion within the skin. In PV, anti-dsg1/3 autoantibodies disrupt the adhesion between keratinocytes, leading to the separation of skin cells.

The process by which intraepidermal blisters develop is called acantholysis. Clinically, PV is characterized by flaccid blisters and partially crusted, painful erosions on the skin and/or mucous membranes. PV and other autoimmune blistering skin diseases can be potentially life-threatening. Current therapeutic approaches primarily focus on immunosuppressing the patient's immune system.

The aim of my research is to possibly identify ion channel inhibitors, tested in the human skin organ culture model (HSOC), as a new therapeutic option for PV. Using the HSOC model, I aim to evaluate the degree of split formation in the skin in response to various ion channel inhibitors through histological and direct immunofluorescence analyses.