Pemphigus vulgaris (PV) is an autoimmune, intraepithelial, blistering disease affecting the skin and mucous membranes. Autoantibodies (IgG) form against Desmoglein (Dsg) 1 and Dsg 3 causing the keratinocytes to separate, which is also called acantholysis. The loss of cell adhesion leads to intraepithelial blistering of the skin and/ or mucous membranes presenting symptoms such as burning pain, bleeding and dysphagia in humans.

At the moment the therapy of PV consists of systemic administration of steroids and other immunosuppressant drugs, both of which have severe side effects. New insides into the pathogenesis of PV are essential in order to develop and test possible new treatment options for this disease.

In my project I am investigating the pathogenesis of PV in a human skin organ culture (HSOC) model previously established in our lab (Imke Burmester et al., 2019) to mimic the intraepidermal split formation of PV by injecting a single chain variable fragment (scFv). The scFv has been found to form against Dsg 3 and Dsg 1 in an ex vivo skin organ culture in human and murine skin.

My aim is to determine at what time, after injection of the scFv, the split formation occurs within the HSOC and to investigate the proteome of skin samples from the HSOC over a time course of 24 hours. I will also try to visualize the blisters in the intact skin samples from the HSOC using optical coherence tomography in cooperation with the Institute of Biomedical Optics.