Proteinase activation: a mechanism for cellular dyshesion in pemphigus

Abstract

An in vitro model system using cultured newborn epidermal cells was employed to investigate the binding of pemphigus autoantibody and subsequent loss of adhesion between epidermal cells. Pemphigus antibodies bound to both mouse and human cultured epidermal cells. Incubation of cultured newborn mouse epidermal cells with pemphigus antibody followed by gentle agitation induced loss of adhesion between the epidermal cells and the plastic culture dish. Release of viable epidermal cells from the dish was inhibited by the proteinase inhibitors, soybean trypsin inhibitor and alpha 2-macroglobulin. These observations suggest that pemphigus antibody induces viable epidermal cells to activate cellular proteinases which then degrade the glycocalyx and cause cellular dyshesion and acantholysis.