Induction of Pemphigus in Neonatal Mice by Passive Transfer of IgG from Patients with the Disease

TLDR

The study examined whether circulating autoantibodies cause pemphigus vulgaris by passively transferring patient IgG into neonatal mice. IgG fractions from five patients were injected intraperitoneally into neonatal Balb/c mice at 1.5–16 mg g⁻¹ body weight per day. Cutaneous blisters and erosions characteristic of pemphigus developed in 39 of 55 mice receiving patient IgG, but in none of 58 controls; disease severity correlated with IgG titers and was dose‑dependent, confirming that pemphigus autoantibodies can be passively transferred to induce disease. Published in N Engl J Med 1982; 306:1189–96.

Abstract

We examined the role of circulating autoantibodies in the pathogenesis of pemphigus vulgaris by passively transferring IgG fractions from five patients with pemphigus vulgaris into neonatal Balb/c mice, in doses of 1.5 to 16 mg per gram of body weight per day. Cutaneous blisters and erosions with the histologic, ultrastructural, and immunofluorescence features of pemphigus occurred in 39 of 55 mice given intraperitoneal injections of IgG from patients with pemphigus and in none of 58 control mice given normal human IgG. IgG fractions with high titers of pemphigus antibodies were most effective in inducing disease, and this effect was dose dependent. Titers of circulating IgG in mouse serum closely correlated with the extent of disease induced (P<0.002). This study strongly supports the proposed role of pemphigus autoantibodies in the pathogenesis of pemphigus vulgaris in human beings and demonstrates that pemphigus can be passively transferred to laboratory animals. (N Engl J Med. 1982; 306:1189–96.)