LFA-1 and Mac-1 are involved in experimental BP. WT and Mac-1 KO mice were pretreated with PBS or β2 integrin-neutralizing antibody and 2 hours later were injected intradermally with control or pathogenic IgG R530. The mice were examined 24 hours after R530 injection. (A) WT mice injected with R530 (ii), but not injected with control (i) or pretreated with antibody against CD11a (iii), CD11b (iv), both CD11a and CD11b (v), or CD18 (vi) showed no skin lesions. (B) MPO assay showed significantly higher levels of neutrophil infiltration in WT mice (bar 1) than WT mice pretreated with antibody against CD11a (bar 2), CD11b (bar 3), both CD11a and CD11b (bar 4), or CD18 (bar 5). Data shown are the mean ± SEM. n = 8 for each group. (C) R530-injected WT mice developed skin blisters and showed linear deposition of rabbit IgG (ii) and mouse C3 (iii) at the BMZ by direct IF. H&E-stained section from these mice revealed a subepidermal vesicle with neutrophilic infiltrate (iv, inset). In contrast, R530-injected Mac-1 KO mice showed no clinical (v) nor histological (viii) blisters, although direct IF showed rabbit IgG and mouse C3 deposition at the BMZ (vi-vii). Position of the skin lesion (arrow), site of basal keratinocytes (arrowhead), dermis (D), epidermis (E), vesicle (V) (original magnification, × 200). Higher magnifications of H&E-stained sections exhibit infiltrating neutrophils in the dermis (insets), original magnification, × 920. (D) MPO assay revealed a significant decrease in neutrophil accumulation in Mac-1 KO (bar 2) and Mac-1 KO mice pretreated with anti-CD11a antibody (bar 3) compared with WT mice (bar 1). Data shown are the mean ± SEM. n = 9. ^*P < .01; ^**P < .001. P < .05 (bar 2 vs bar 3).