Abstract

Three lines of evidence support a role for antibody in the induction of acantholysis in pemphigus: correlation of antibody titers with disease activity, induction of acantholytic lesions in neonatal mice by passive transfer of patient IgG, and induction of acantholytic lesions in explants of normal human skin following incubation with patient IgG in the presence and absence of plasminogen. The authors discuss all three lines of evidence and describe the model they have developed in vivo to explain induction of acantholytic lesions by antibody.

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