Immunoglobulin G (IgG) autoantibodies are major drivers of inflammation and tissue destruction in pemphigoid diseases. While lowering IgG half-life via generally blocking FcRn function is a promising strategy to diminish autoantibody pathology, this approach is non-selective and also results in a reduction of protective antibody species. Thus, the main goal of project A07 is to understand to what extent cellular neighbourhoods in the skin, consisting of immune and non-immune cells, contribute to autoantibody-triggered skin pathology via FcRn. Understanding FcRn function locally may allow a more specific targeting of FcRn in the future.