ABSTRACT
The flaky skin (fsn) mouse mutation arose as a spontaneous mutation in the A/J inbred strain at the Jackson Laboratory in 1985. The flaky skin mutation is currently on the N8F2 generation toward inbreeding the fsn gene onto the BALB/cByJ background and the N9F3 generation toward inbreeding on the C57BL/6J background. The major alterations included diminished tonofibrils, poor fusion of tonofilaments to keratohyalin granules, intercellular lipid vacuoles in the stratum corneum, and tortuous dermal blood vessels lined by a hyperplastic endothelium with a multilaminated basement membrane, all features described in human psoriatic lesions. This chapter suggests that epidermal trauma, even during early stages of the disease, stimulates the development of skin lesions (Dunstan and Sundberg, unpublished data). It repeats using topical applications of cyclosporin A on both fsn/fsn and nu/nu mice and their littermate controls. It concludes that cyclosporin A was not effective in treating the epidermal hyperplasia in fsn/fsn mice by the routes or doses administered.
