Analysis of pathomechanism of blister formation in pemphigus vulgaris using post-embedding immuno-electron microscopy

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In order to give an insight into the pathophysiological mechanism of blister formation in pemphigus vulgaris, we performed ultrastructural experiments using novel monoclonal antibodies against dsg3 injected into organ-cultured human skin. A monoclonal antibody having ability to induce blister reached extracellular surface of desmosomes in all layers of epidermis within 2 hours, but did not induce acantholysis yet. After 22 hours, acantholysis developed and desmosomal structures and dsg3 molecules were disappeared from the keratinocytes cell surface. Some amount of dsg3 were detected in the cytoplasm. Using non-pathogenic monoclonal antibody instead of the pathogenic antibody, nothing of above mentioned changes were observed. These results suggest both steric hinderans and dsg3 internalization occurs in our system within 22 hours, although more precise time-course observation is expected to show dynamic mechanism of blister formation.