FULL-THICKNESS SKIN-GRAFTS FROM FLAKY SKIN MICE TO NUDE-MICE - MAINTENANCE OF THE PSORIASIFORM PHENOTYPE

Flaky skin (fsn) is an autosomal recessive mouse mutation with papulos quamous disease features similar to human psoriasis. In fsn/fsn skin, one sees marked acanthosis and hyperkeratosis with focal parakeratosis , subcorneal pustules, dermal capillary dilation, and a marked diffuse dermal infiltration of mixed inflammatory cells, predominantly lympho cytes. To determine if these pathologic features are a characteristic of the skin or a chronic autoimmune attack, we laced full-thickness sk in grafts from affected homozygous (fsn/fsn) and normal littermate con trol (+/?) mice on the dorsal skin of genetically athymic nude (nu/nu) mice. After 10 weeks of observation, the grafts maintained the histol ogic phenotype of the donor animal. In the fsn/fsn grafts, there was p ersistence of both epidermal proliferation and dermal inflammation, ch aracteristics of the mutation. The fsn/fsn phenotype was also confirme d by immunohistochemical evaluation for specific mouse keratinocyte ma rker expression. Based on tritiated thymidine uptake, we found DNA syn thesis rates elevated threefold or more in fsn/fsn epidermis compared to littermate control mouse skin. Elevated rates of DNA synthesis rema ined a feature of the fsn/fsn grafts but not that of littermate contro l skin grafts. This study demonstrates that the psoriasiform phenotype of this mouse mutation can persist independent of the host thymic-der ived immune system.