C5AR2 and acquired epidermolysis bullosa: In contrast to the protective role of C5aR2 in experimental BP, C5aR2-deficient mice developed an attenuated disease phenotype in the antibody transfer mouse model of EBA, with C5aR2 being essential for neutrophil activation and recruitment by regulating Fcγ receptor (FcγR) expression levels in this model (59, 87).