Cole, ConnorConnorColeVinay, KeshavamurthyKeshavamurthyVinayBorradori, LucaLucaBorradoriAmber, Kyle TKyle TAmber2024-10-112024-10-112022-07https://boris-portal.unibe.ch/handle/20.500.12422/86336Bullous pemphigoid is an autoimmune blistering disease caused by autoantibodies targeting BP180 and BP230. While deposits of IgG and/or complement along the epidermal basement membrane are typically seen suggesting complement -mediated pathogenesis, several recent lines of evidence point towards complement-independent pathways contributing to tissue damage and subepidermal blister formation. Notable pathways include macropinocytosis of IgG-BP180 complexes resulting in depletion of cellular BP180, direct induction of pro-inflammatory cytokines from keratinocytes, as well as IgE autoantibody- and eosinophil-mediated effects. We review these mechanisms which open new perspectives on novel targeted treatment modalities.enBP180 BP230 autoimmune blistering diseases bullous pemphigoid complement - immunological terms eosinophils – immunology igE (Immunoglobulin E)600 - Technology::610 - Medicine & healtharticle10.48350/1715353587474510.3389/fimmu.2022.912876