Pemphigus vulgaris (PV) is a rare and potentially life-threatening autoimmune blistering disease affecting the skin and surface-close mucous membranes. PV is characterized by autoantibodies against the desmosomal antigen molecules desmoglein (Dsg) 1 and 3. In addition to directly disrupting desmosomal adhesion, binding of pemphigus IgG activates intracellular signaling pathways that indirectly contribute to acantholysis and disease progression.

This PhD project aims to elucidate the role of kinase-mediated signaling pathways in the pathogenesis of PV using an established adult mouse model of PV. The project will evaluate the therapeutic efficacy of selected kinase inhibitors in reducing disease progression and compare their effectiveness with current standard treatments. In addition, multi-omics approaches will be employed to identify disease-associated molecular signatures and signaling networks. These analyses may provide insights into early pathogenic events, support the identification of predictive biomarkers, and contribute to the development of personalized therapeutic strategies for PV and related conditions.