Figure 2

Prophylactic TNF blockade reduced the extent of skin disease in antibody transfer-induced EBA. Mice injected with rabbit anti-mCOL7C IgG and treated with (A,B) an isotype antibody (n = 8) or (C,D) a monoclonal antibody to TNF (TNF mAb, n = 6) 2 d prior to initial anti-mCOL7C IgG injection, followed by five treatments every other day until d 8. Ears and trunks of isotype-treated mice demonstrated erythema and erosions, while less disease was observed in TNF mAb-treated mice. (E) Time course of clinical disease development, shown as the percentage of body surface area affected by blistering (*p < 0.05, **p < 0.01). Representative ear samples from (F–J) isotype-treated and (K–O) TNF mAb-treated mice with EBA were analyzed histopathologically and immunologically. By direct immunofluorescence microscopy, similar (F,K) IgG and (G,L) C3 deposits were observed at the dermal-epidermal junction in both experimental groups. Histopathological analysis of lesional skin demonstrated comparable (H,M) dermal-epidermal separation in both treatment groups, but (I,N) TNF and (J,O) MOMA-2 were detected to a lesser extent in (N,O) TNF mAb-treated mice compared with (I,J) isotype-treated mice. Magnification of all sections is 200×.