Although it is accepted that pemphigus antibody binding to keratinocytes (KCs) evokes an
array of intracellular biochemical events resulting in cell detachment and death, the
triggering events remain obscure. It has been postulated that the binding of pemphigus
vulgaris IgG (PVIgG) to KCs induces" desmosomal" signaling. Because in contrast to
integrins and classical cadherins, desmoglein (Dsg) molecules are not known to elicit
intracellular signaling, and because PV patients also produce non-Dsg autoantibodies, we …