Caspase-activation powers anti-Desmoglein 3-induced acantholysis in human epidermis.

ABSTRACT: Pemphigus vulgaris (PV) is a life-threatening autoimmune blistering disease caused by circulating autoantibodies against desmoglein (Dsg) 1 and Dsg 3. Whether acantholysis in PV results exclusively from antibody binding to Dsgs or involves additional factors remains controversial. Given that Fas-Ligand (FasL), an activator of apoptotic caspase-8, is increased in the serum and the skin of patients with PV, we investigated the role of caspases in anti-Dsg3-mediated acantholysis using both ex vivo and in vitro models. Our results demonstrated that anti-Dsg3 antibodies induced acantholysis ex vivo in the absence of caspase activation, primarily through the redistribution of Dsg3 to intracellular compartments. FasL-induced caspase activation led to a synergistic amplification of anti-Dsg3-media

SUBMITTER: Schmidt MF 

PROVIDER: S-EPMC12949151 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature