Pemphigus vulgaris (PV) is an autoimmune disease characterized by epidermal blistering involving mucosa or mucosa and skin (Ding et al., 1997). In PV, autoantibodies directed against the desmosome cadherins desmoglein (dsg) 3 and dsg1 induce loss of cell–cell adhesion (acantholysis) resulting in clinical blisters. Passive transfer experiments using IgG, purified from PV patients (Anhalt et al., 1982) or highly specific anti-dsg3 monoclonal antibodies (Tsunoda et al., 2003; Payne et al., 2005), reproduce the clinical, histologic, and immunologic features of PV in the infused animals. Similarly, pemphigus foliaceus (PF) is an autoimmune blistering disease of the skin in which autoantibodies to dsg1 cause acantholysis in the subcorneal and granular layers of the epidermis. IgG purified from PF patient sera similarly reproduces disease in the passive transfer mouse model (Roscoe et al., 1985;