FIG. 8.

RelA/c-rel-deficient skin grafts develop TNF-α-dependent epidermal hyperplasia. Skin from E18 control (rela^+/+ c-rel^−/− tnfα^−/−) and mutant (rela^−/− c-rel^−/− tnfα^−/−) fetuses was grafted onto C57BL/6 rag-1^−/− mice (A, Bi to iv, and Ci to iv) or C57BL/6 rag-1^−/− tnfα^−/− mice (Di to v). (A) Appearance of representative donor skin grafts over a 4-week period. (B and C) Histological analysis of skin grafts on C57BL/6 rag-1^−/− recipients is representative of four control and three mutant skin grafts. H&E-stained sections from control (Bi) and mutant (Bii) skin grafts were analyzed under low power at 4 weeks. Bar, 1,600 μm. Staining for keratin-6 was confined to hair follicles in the control graft (Biii) and the epidermis in the mutant graft (Biv). Bar, 425 μm. High-power analysis of H&E-stained sections revealed pockets of dermal infiltrate (arrow) in the mutant graft (Ci) that were mostly eosinophilic (asterisks) and granulocytic (arrowhead) (Cii). Bar, 225 μm. Note red cytoplasmic staining of eosinophils. Pearl staining for melanin on paraffin sections of control (Ciii) and mutant (Civ) grafts. (D) Skin grafts on C57BL/6 rag-1^−/− tnfα^−/− recipients at 4 weeks is representative of three control and three mutant grafts. H&E-stained sections from control (Di) and mutant (Dii) grafts were analyzed at low power. Bar, 1,600 μm. Some dermal infiltrate (fibroblasts and macrophages; asterisks) was observed in the mutant graft (Diii). Three major hair types (tyrlotrich, awl, and zigzag) were observed in the control graft (Div), while only two (awl and zigzag) were evident in the mutant graft (Dv). Note that the mutant hairs are thinner.