Abstract

Pemphigus vulgaris is characterized by suprabasal splitting of the epithelium and loss of intercellular attachments. In order to clarify the molecular mechanism of blister formation in oral mucosa in pemphigus vulgaris, we further analyzed the effects of pemphigus serum on the distribution of keratin intermediate filaments and also on that of desmoplakin I, II which is one of the components of desmosome, major attachment apparatus between keratinocytes. After incubation with pemphigus serum for 96 hrs at 37°C, we observed a dotted structure around the nucleus using anti-keratin monoclonal antibodies (PKK1, PKK2, PKK3 and anti-cytokeratin pan) in some of the cells from normal gingiva, and some decrease in fibrous radiating structures as we previously reported. All of anti-keratin monoclonal antibodies we used stained this dotted structure, although PKK2 stained most clearly them as well as fibrous structure among antibodies. Similar dotted staining was also observed when antidesmoplakin I, H monoclonal antibody was applied.These results suggest that the binding of pemphigus antibody to keratinocyte membrane induced the structural changes in keratin intermediate filaments, also in desmosomes, and a complex of them. We consider that these phenomena might be a characteristic feature of oral keratinocytes.

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