Is there an emergent need to modify the Desmoglein compensation theory in pemphigus on the basis of ELISA data and alternative pathogenic mechanisms ?

We read with interest the study by Koga H et al and we believe that in light of recent observations including our data the

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desmoglein compensation theoryas a explanation for localization of blisters should be revisited. Although the disruption of desmoglein-dependent cell adhesion by autoantibodies is the basic pathophysiology underlying blister formation in pemphigus, the clinical spectrum does not always mirror this pathogenic process. Three clinical types of pemphigus have been described, the mucosal dominant, cutaneous and mucocutaneous type.

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