Autoimmunity occurs when the immune system attacks its own healthy cells and tissues leading to an aberrant immune response on the body. The development of autoimmune diseases is dependent on different environmental factors like smoking, age, gender, and psychosis. Many autoimmune diseases like autoimmune bullous dermatoses are mediated by autoantibodies.

Pemphigoid diseases are a subgroup of acute or chronic autoimmune skin disorders that could be life-threatening for the patients, characterized and caused by autoantibodies directed against structural components of the dermal-epidermal junction. The autoantibodies bind to those components leading to the formation of blisters and erosions in patients. Epidermolysis bullosa acquisita (EBA) is a rare, subepidermal blistering disease. EBA is characterized by autoantibodies to collagen VII, which serves to link the epidermis to the dermis, leading to severe blistering and crust formation.

EBA is currently mostly studied using the rabbit anti-mouse antibody transfer-induced mice model. Although this model is well established and commonly used, it comes with disadvantages. First of all, there is only one subclass of rabbit IgG compared to the 4 subclasses of the mice IgG. Moreover, since it is produced by a different organism it induces an immunological reaction irrelevant to EBA and has a high cost due to the need of rabbits for the production.

We want to develop a new antibody transfer-induced mouse anti-mouse model for EBA and afterward, investigate whether the glycosylation profile and epitope specificity plays a role to the pathogenicity of the antibodies.