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

Figure 8.

Figure 8

Contribution of FcγRII to HDIG-induced degradation of pathogenic IgG. WT and FcγRII–/– mice were injected i.p. with pathogenic anti-BP180 (25 μg/g body weight), anti-Dsg1 (40 μg/g body weight), or anti-Dsg3 (50 μg/g body weight) IgG with buffer or HDIG (1 mg/g body weight) pretreatment. Mice were examined clinically, and the levels of circulating pathogenic anti-mBP180, anti-Dsg1, and anti-Dsg3 antibodies were quantified 48 hours after IgG injection. HDIG treatment caused a similar degree of reduction in circulating pathogenic IgG levels and blocked clinical blister formation in both WT and FcγRII–/– mice. IgM control (6.47 mg/g body weight) showed results similar to those for buffer control (Table 2). n = 6 in each group.