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

Figure 3.

Figure 3

FcRn-deficient mice are resistant to experimental BP. Neonatal WT and FcRn–/– mice were injected i.p. with pathogenic anti-mBP180 IgG or normal rabbit IgG control (25 μg/g body weight) and examined 48 hours after injection. WT mice receiving pathogenic IgG developed clinical (A) and histological (C) evidence of subepidermal blisters. Direct IF exhibited in vivo deposition of rabbit anti-mBP180 IgG at the basement membrane (B). In contrast, FcRn–/– mice showed no skin lesions (D and F) and very weak IgG deposition at the basement membrane (E). (G) The MPO assay showed a significant reduction in neutrophil infiltration in FcRn–/– mice relative to WT mice. (H) ELISA assay revealed a significant acceleration of pathogenic IgG degradation in FcRn–/– mice. n = 6. *P < 0.01. Arrow indicates site of pathogenic antibody binding.