作者: H. HogenEsch , C. Zurcher , M.J.J. Gijbels , J. van Hooft , E. Offerman
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摘要: Chronic proliferative dermatitis is a new spontaneous mutation in C57BL/Ka mice. Breeding results suggest an autosomal recessive mode of inheritance. Mutant mice develop skin lesions at the age 5 to 6 weeks. The occur ventral and dorsal body, whereas ears, footpads, tail are not involved. characterized by epidermal hyperplasia, hyper- parakeratosis, single cell necrosis keratinocytes. dermis epidermis infiltrated granulocytes macrophages, occasionally subcorneal intracorneal microabscesses formed. number mast cells progressively increases with age. There dilatation proliferation dermal capillaries. Similar mouth, esophagus, forestomach, which, mouse, all lined orthokeratinizing stratified squamous epithelium. Studies bromodeoxyuridine confirm increased rate epithelial proliferation. Most inflammatory affected express Mac-1, few T lymphocyte marker CD3. expression intercellular adhesion molecule-1 on keratinocytes endothelial cells. Infiltration neutrophils macrophages also seen liver, lung, several joints. disease could be transferred bone marrow or spleen transplants into irradiated normal syngeneic hosts. Treatment triamcinolone, long-acting corticosteroid, resulted nearly complete regression over period 4 weeks, systemic cyclosporin A treatment was ineffective. Chemicals/CAS: broxuridine, 59-14-3; A, 59865-13-3, 63798-73-2; molecule 1, 126547-89-5; 124-94-7; Adrenal Cortex Hormones; Cyclosporine, 59865-13-3