| First Author | Sundberg JP | Year | 1994 |
| Journal | J Invest Dermatol | Volume | 102 |
| Issue | 5 | Pages | 781-8 |
| PubMed ID | 8176263 | Mgi Jnum | J:18002 |
| Mgi Id | MGI:66024 | Doi | 10.1111/1523-1747.ep12377741 |
| Citation | Sundberg JP, et al. (1994) Full-thickness skin grafts from flaky skin mice to nude mice: maintenance of the psoriasiform phenotype. J Invest Dermatol 102(5):781-8 |
| abstractText | Flaky skin (fsn) is an autosomal recessive mouse mutation with papulosquamous 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 lymphocytes. To determine if these pathologic features are a characteristic of the skin or a chronic autoimmune attack, we placed full-thickness skin grafts from affected homozygous (fsn/fsn) and normal littermate control (+/?) mice on the dorsal skin of genetically athymic nude (nu/nu) mice. After 10 weeks of observation, the grafts maintained the histologic phenotype of the donor animal. In the fsn/fsn grafts, there was persistence of both epidermal proliferation and dermal inflammation, characteristics of the mutation. The fsn/fsn phenotype was also confirmed by immunohistochemical evaluation for specific mouse keratinocyte marker expression. Based on tritiated thymidine uptake, we found DNA synthesis rates elevated threefold or more in fsn/fsn epidermis compared to littermate control mouse skin. Elevated rates of DNA synthesis remained a feature of the fsn/fsn grafts but not that of littermate control skin grafts. This study demonstrates that the psoriasiform phenotype of this mouse mutation can persist independent of the host thymic-derived immune system. |
