Pemphigus is a severe autoimmune disease caused by autoantibodies against desmogleins (Dsgs). Dsgs are proteins that are part of desmosomes, desmosomes are part of cell-cell-contacts. The destruction of Dsgs and therefore desmosomes causes intraepidermal blisters in a process called acantholysis. There are several forms of pemphigus. They differentiate from each other by the Dsgs the antibodies bind to.

The most common form is pemphigus vulgaris (PV). PV is divided into two main sub forms:

(1)   One is mucous PV where patients show mucosal blistering due to anti-Dsg3 antibodies.

(2)   The other form is mucocutaneous PV (mcPV) where patients suffer from mucosal and skin erosions because of anti-Dsg3 and anti-Dsg1 antibodies.

Additionally, there have also been found antibodies against other targets in PV patients recently, especially with mcPV.   The aim of this project is to find antibodies, that bind to other targets than Dsgs in a phage library of a mcPV patient by using antibody phage display. Afterwards we will use several methods to characterize these antibodies. We would like to find out whether these non-Dsg antibodies induce acantholysis on their own or enhance the pathogenicity of anti-Dsg antibodies.