Pemphigoid diseases (PD) exhibit a relapsing-remitting disease pattern and a preferential affection of certain skin parts, suggesting that local cell populations facilitate regional inflammation. Our preliminary data suggest that dermal fibroblasts (DFs) get metabolically and functionally “primed” by repeated inflammation in the passive transfer model of epidermolysis bullosa acquisita and mediate progressive worsening. In project B10, we will delineate the priming response of the skin and focus on mouse and human DFs and their interaction with PD-relevant inflammatory cells.  We will also try to “un-prime” DFs by interfering with candidate pathways differentially regulated in primed DFs.