Pemphigus foliaceus (PF) is a dermatosis characterized by subcorneal v
esicles and pathogenic IgG autoantibodies against desmoglein 1, PF IgG
passively transferred into neonatal mice induces a blistering disease
that duplicates the key findings of PF. In this study we have used th
is animal model to investigate the role of complement and IgG; valence
in triggering blister formation. In the passive transfer experiments,
we found that PF IgG, as well as the F(ab')(2) and Fab fragments, was
capable of inducing the typical subcorneal blistering disease in both
complement-deficient and complement-sufficient mice. Morever, the dis
ease activity in these mice correlated well with the dose of IgG or it
s proteolytic fragments injected in the animals. We conclude that neit
her complement activation nor IgG-mediated cell surface antigen crossl
inking is required for the induction of acantholysis in the experiment
al PF model. (C) 1997 Academic Press.