Abstract
Pemphigus is a rare autoimmune disease, involving the skin and mucous epithelia, characterized by flaccid blisters and erosions. Histologically, the basic abnormality in all forms of pemphigus is the separation of keratinocytes from one another, a process known as acantholysis. There is direct evidence that autoantibodies against desmoglein, a transmembrane desmosomal component, are critical in its pathogenesis, but the exact mechanism that induces acantholysis is yet unknown. Actually, different studies suggest three possible mechanisms: sterical impedance, intracellular signalling and apoptosis. Understanding these processes should show new therapeutic perspective.
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