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

Posté le September 13, 2012 par Cristo Rey Intern

We read with interest the study by Koga H et al¹ and we believe that in light of recent observations including our data (Table 1) the “desmoglein compensation theory” as a explanation for localization of blisters should be revisited ^2,3,4. Although the disruption of desmoglein-dependent cell adhesion by autoantibodies is the basic pathophysiology underlying blister formation in pemphigus ²⁻⁴, 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 ^2,,3,4 .
http://onlinelibrary.wiley.com/doi/10.1111/bjd.12012/abstract

Tagués avec : auto-anticorps, library, pathophysiology, pemphigus
Publié dans Dans le monde entier, Actualités et informations