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

Figure 4.

Figure 4

FcRn-deficient mice are resistant to experimental PF and PV. Neonatal WT and FcRn–/– mice were injected i.p. with pathogenic anti-Dsg1 (PF1, 40 μg/g body weight) (A–C) or anti-Dsg3 (PV1, 50 μg/g body weight) (D–F) IgG and examined 48 hours after injection. (A–C) PF model. WT mice receiving pathogenic IgG developed subcorneal blisters (A), while FcRn–/– mice showed no skin lesions (B). (C) ELISA revealed a significant reduction in circulating anti-Dsg1 IgG levels in FcRn–/– as compared with WT mice. (D–F) PV model. WT mice receiving pathogenic IgG developed suprabasal blisters (D), while FcRn–/– mice showed no skin lesions (E). (F) ELISA revealed a significant reduction in circulating anti-Dsg3 IgG levels in FcRn–/– as compared with WT mice. n = 8. *P < 0.01. Arrow indicates basal keratinocytes.