A key step in the pathogenesis of epidermolysis bullosa acquisita (EBA) is the development of anti-hCOL7 antibodies directed against collagen type VII, which serves as an anchor fibril between the epidermis and the dermis. Activation of neutrophils by COL7/anti-hCOL7 immunocomplexes lead to complement activation and reactive oxygen species (ROS) release, resulting in split formation at the dermal-epidermal junction. This becomes visible as blistering of the skin.^1,2 Pathogenicity of autoantibodies depends on the antibody subclass. ² Within the same subclass, cellular functions and inflammatory activity of the neutrophils are determined by the sugar moiety attached to the antibodies.³ In my project, I will investigate the kinome signature in neutrophils activated by differentially glycosylated IgG4 immunocomplexes. Furthermore, I will determine specific kinase activity by measuring the phosphorylation of kinases by Western blot. The most important cellular function will be the release of ROS, which will be measured by a luminescence-based assay.