Epidermolysis bullosa aquisitia is a severe autoimmune blistering disease that belongs to the group of pemphigoid diseases. As a crucial step in the pathomechanism of EBA, autoantibodies (primarily IgG) target type VII collagen, an adhesion protein of the dermal-epidermal junction (DEJ)¹.

Pathogenic immune complexes (ICs) consisting of the autoantigene type VII collagen and autoantibodies (e.g. IgG1-4) induce activation of neutrophils by activating Fcγ receptors (FcγRs)².

The extent of the subsequent signalling is affected by different subclasses and glycosylation patterns of the IgG antibodies. As a result of their activation, neutrophils release reactive oxygen species (ROS) which directly contribute to split formation at the DEJ and therefore skin blistering.

The overarching aim of my project is to identify kinase signatures and cellular functions in neutrophils activated with different IgG subclasses and glycosylation patterns. In the context of autoimmune pre-disease, knowledge of the exact impact of the different IgG subclasses on the kinome and the effector function of neutrophils can help to understand the outbreak of the disease and to find possibilities to circumvent it.