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. 2005 Nov 10;115(12):3440–3450. doi: 10.1172/JCI24394

Figure 1.

Figure 1

High-dose Ig inhibits experimental BP by accelerating degradation of pathogenic anti-mBP180 IgG. Neonatal C57BL/6J mice were pretreated with buffer, IgM (12.93 mg/g body weight), or different doses of HDIG (0–2 mg/g body weight) and injected i.p. with pathogenic IgG (25 μg/g body weight) 2 hours later. The animals were examined 48 hours after pathogenic IgG injection. Control mice showed typical BP clinically (A) and histologically (B). In contrast, mice pretreated with HDIG were protected from BP, and the protective effect was dose dependent (C–F). (G) HDIG treatment resulted in significant reduction in clinical skin disease (bars 3–5) as compared with IgM (bar 1) and buffer controls (bar 2). (H) MPO assays revealed a significant reduction in neutrophil infiltration in mice treated with HDIG (bars 3–5) as compared with control mice (bars 1 and 2). (I) ELISA showed a similar pattern of reduction in circulating pathogenic IgG in mice treated with HDIG (bars 3–5) relative to controls (bars 1 and 2). n = 8 in each group. *P < 0.05; **P < 0.001. e, epidermis; d, dermis; v, vesicle. Arrow indicates site of pathogenic antibody binding.