The decline of mitochondrial metabolism in lymphocytes is tightly correlated with age due to an accumulation of mutations in the mitochondrial genome. Pemphigoid diseases (PDs) are typical autoimmune diseases of the elderly. However, it remains unknown how mitochondrial metabolism controls autoimmunity in PDs. In this project, we aim to define the regulatory circuits that connect mitochondrial metabolism, immune cell signaling and their effector functions in PDs and explore, if pharmacological modulation of selected mitochondrial pathways is a feasible strategy to treat the immunopathology in PD patients.