Fig. 7.
Fig. 7. Skin histological studies of triple-mutant, E/P double-mutant, and control mice. / Skin sections were obtained from the area of the neck where lesions formed (Figure 6). Cervical skin from wild-type (A) and L-selectin–deficient (B) mice was normal and without lesions. (C) Skin from 15-month-old E/L/P triple mutants was essentially normal. (D) Cervical skin from E/P double-mutant mice was diffusely ulcerated, with the surface colonized by bacteria and a mixed acute and chronic inflammatory infiltrate that disrupted the underlying dermis and pannicular skeletal muscle layer. (E) Section of an excoriative skin lesion representative of the lesions that developed in the 3 most severely affected triple-null mice. Lesions that formed in the few triple-null mice affected were much less severe than those common in the E/P double-mutant mice, with the underlying structural layers remaining intact (hematoxylin and eosin, original magnification × 200).

Skin histological studies of triple-mutant, E/P double-mutant, and control mice.

Skin sections were obtained from the area of the neck where lesions formed (Figure 6). Cervical skin from wild-type (A) and L-selectin–deficient (B) mice was normal and without lesions. (C) Skin from 15-month-old E/L/P triple mutants was essentially normal. (D) Cervical skin from E/P double-mutant mice was diffusely ulcerated, with the surface colonized by bacteria and a mixed acute and chronic inflammatory infiltrate that disrupted the underlying dermis and pannicular skeletal muscle layer. (E) Section of an excoriative skin lesion representative of the lesions that developed in the 3 most severely affected triple-null mice. Lesions that formed in the few triple-null mice affected were much less severe than those common in the E/P double-mutant mice, with the underlying structural layers remaining intact (hematoxylin and eosin, original magnification × 200).

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