Blistering autoimmune dermatosies (BAID) are rare, acquired skin disorders caused by autoantibodies against structural proteins crucial for keratinocyte adhesion and epidermal-dermal attachment. Besides the ksin, mucous membranes can also be affected. BAID are divided into two groups: pemphigus diseases, with intraepidermal blisters due to antibodies against desmosomal proteins (e.g. desmoglein ⅓), and subepidermal BAID, with blistering at the dermoepidermal junction, targeting proteins susch as BP180, BP230, laminin 33, a6ß4-integrin, and type VII collagen. Supepidermal BAID include bullous pemphigoid, mucous membrane pemphigoid, pemphigoid gestationis, linear IgA dermatosis, epidermolysis bullosa acquisita, and others. 

Diagnosis of BAID relies on detecting tissue-bound and/or circulating autoantibodies, with direct immunofluorescence (DIF) as gold standard. Further differentiation uses indirect immunofluorescence on salt-split skin, ELISA, biochips, and immunoblotting.

This project focuses on sera binding to the epidermal siede of salt-split skin without known antigen specificity. These may represent atypical or novel disease variants or ealry stages of defined BAID. Aim of the study is to identify additional target antigens to improve understanding of early pathogenic mechanisms and autoantibody responses, thereby supporting the development of new therapeutic strategies.