TY - JOUR
T1 - A spontaneous mutation characterized by chronic proliferative dermatitis in C57BL mice
AU - HogenEsch, H.
AU - Gijbels, M. J.
AU - Offerman, E.
AU - van Hooft, J.
AU - van Bekkum, D. W.
AU - Zurcher, C.
PY - 1993
Y1 - 1993
N2 - 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 of 5 to 6 weeks. The lesions occur in the ventral and dorsal skin of the body, whereas ears, footpads, and tail are not involved. The lesions are characterized by epidermal hyperplasia, hyper- and parakeratosis, and single cell necrosis of keratinocytes. The dermis and epidermis are infiltrated by granulocytes and macrophages, and occasionally subcorneal and intracorneal microabscesses are formed. The number of mast cells in the dermis progressively increases with age. There is dilatation and proliferation of dermal capillaries. Similar lesions develop in the mouth, esophagus, and forestomach, which, in the mouse, are all lined by orthokeratinizing stratified squamous cell epithelium. Studies with bromodeoxyuridine confirm the increased rate of epithelial cell proliferation. Most inflammatory cells in the affected skin express Mac-1, and few express the T lymphocyte marker CD3. There is increased expression of intracellular adhesion molecule-1 on keratinocytes and endothelial cells. Infiltration of neutrophils and macrophages are also seen in the liver, lung, and several joints. The disease could not be transferred by bone marrow or spleen transplants into irradiated normal syngeneic hosts. Treatment of the mice with triamcinolone, a long-acting corticosteroid, resulted in nearly complete regression of the lesions over a period of 4 weeks, whereas systemic cyclosporin A treatment was ineffective
AB - 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 of 5 to 6 weeks. The lesions occur in the ventral and dorsal skin of the body, whereas ears, footpads, and tail are not involved. The lesions are characterized by epidermal hyperplasia, hyper- and parakeratosis, and single cell necrosis of keratinocytes. The dermis and epidermis are infiltrated by granulocytes and macrophages, and occasionally subcorneal and intracorneal microabscesses are formed. The number of mast cells in the dermis progressively increases with age. There is dilatation and proliferation of dermal capillaries. Similar lesions develop in the mouth, esophagus, and forestomach, which, in the mouse, are all lined by orthokeratinizing stratified squamous cell epithelium. Studies with bromodeoxyuridine confirm the increased rate of epithelial cell proliferation. Most inflammatory cells in the affected skin express Mac-1, and few express the T lymphocyte marker CD3. There is increased expression of intracellular adhesion molecule-1 on keratinocytes and endothelial cells. Infiltration of neutrophils and macrophages are also seen in the liver, lung, and several joints. The disease could not be transferred by bone marrow or spleen transplants into irradiated normal syngeneic hosts. Treatment of the mice with triamcinolone, a long-acting corticosteroid, resulted in nearly complete regression of the lesions over a period of 4 weeks, whereas systemic cyclosporin A treatment was ineffective
M3 - Article
C2 - 8362989
SN - 0002-9440
VL - 143
SP - 972
EP - 982
JO - American journal of pathology
JF - American journal of pathology
IS - 3
ER -