Mouse models of autoimmune blistering diseases induced by the passive transfer of antibodies.

Passive transfer of IgG into neonatal mice is a potential method of reproducing antibody-mediated blistering skin diseases. The major autoantigen for bullous pemphigoid is collagen XVII (COL17)/BP180, which is an epidermal linker transmembrane protein. A single intraperitoneal injection of human or rabbit IgG against pathogenic epitopes for COL17 can induce skin fragility in neonatal mice that express human COL17. Since amino acid sequences of the pathogenic epitopes for COL17 significantly differ between humans and rodents, the required antibodies are those that correctly target the molecule to induce the blistering phenotype.