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

Figure 2.

Figure 2

HDIG inhibits experimental PF and PV by accelerating degradation of pathogenic human autoantibody 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 anti-Dsg1 IgG (PF1, 40 μg/g body weight) or anti-Dsg3 IgG (PV1, 50 μg/g body weight) 2 hours later. The animals were examined 48 hours after pathogenic IgG injection. Mice without HDIG treatment developed subcorneal PF blisters (A and B), while 1 mg HDIG completely blocked skin lesions (C and D). (E) HDIG treatment resulted in significant reduction in clinical disease scores and levels of circulating anti-Dsg1 IgG (bars 3–5) as compared with control (bars 1 and 2). Mice without HDIG treatment developed suprabasal PV blisters (F and G), while 1 mg HDIG completely blocked skin lesions (H and I). (J) HDIG treatment resulted in significant reduction in clinical disease scores and levels of circulating anti-Dsg3 IgG (bars 3–5) relative to control (bars 1 and 2). n = 8. *P < 0.05; **P < 0.001. Arrows indicate basal keratinocytes.