How is pathogenesis of Pemphigus?

• Blisters in pemphigus vulgaris are associated with the binding of IgG autoantibodies to keratinocyte cell surface molecules (desmoglein 1 and 3) • These antibodies bind to keratinocyte desmosomes and to desmosome-free areas of the keratinocyte cell membrane • The binding of autoantibodies results in a loss of cellto-cell adhesion, a process termed acantholysis • The antibody alone is capable of causing blistering without complement or inflammatory cells