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

Figure 5.

Figure 5

No further degradation of pathogenic IgG by HDIG in FcRn-deficient mice. WT and FcRn–/– mice were pretreated with buffer control, IgM control (6.47 mg/g body weight), or HDIG (1 mg/g body weight) and then injected i.p. with pathogenic anti-BP180 IgG (25 μg/g body weight), anti-Dsg1 IgG (PF1, 40 μg/g body weight), or anti-Dsg3 IgG (50 μg/g body weight). Pathogenic IgG levels in circulation at different time points after pathogenic IgG injection were quantified by ELISA. (A) BP model. Significantly higher levels of circulating anti-BP180 IgG were present in WT mice without HDIG treatment than WT mice with HDIG treatment at 12, 24, and 48 hours. In contrast to WT mice, FcRn-deficient mice with and without HDIG treatment showed similar levels of circulating anti-BP180 IgG. IgM pretreatment had no effect on the serum anti-mBP180 IgG levels at all time points examined (1.04 ± 0.11, 2.47 ± 0.34, 2.09 ± 0.32, and 2.16 ± 0.29 OD492nm reading units at 6, 12, 24, and 48 hours, respectively). (B) PF model. HDIG treatment resulted in significantly reduced levels of anti-Dsg1 IgG in WT mice but not in FcRn–/– mice 48 hours after injection as compared with control IgM-treated WT mice. (C) PV model. As in the PF model, HDIG caused a significant reduction in circulating anti-Dsg3 IgG levels in WT but not in FcRn–/– mice 48 hours after injection. These data show that increased degradation of pathogenic IgG is mainly dependent upon the FcRn-mediated pathway. n = 6. *P < 0.05; **P < 0.001.