Cassian Sitaru

TL;DR: It is strongly suggested that elastase and gelatinase B are essential for granulocyte‐mediated proteolysis resulting in dermal–epidermal separation in EBA and BP patients' skin.

TL;DR: Generally, decisive progress has been made in the characterization of the mechanisms of blister formation in autoimmune skin diseases, however, various aspects, including the exact contribution of steric hindrance and signal transduction for pemphigus IgG‐induced acantholysis or the fine tuning of the inflammatory cascade triggered by autoantibodies in some subepidermal blistering diseases still need to be addressed.

TL;DR: A robust experimental system that reproduces in mice the clinical, histopathological, and immunopathological findings in EBA patients should greatly facilitate further studies on the pathogenesis of EBA and the development of novel immunomodulatory therapies for this and other autoimmune diseases.