title: Development of atopic dermatitis-like skin lesion with IgE hyperproduction in NC/Nga mice.
abstract: Atopic dermatitis (AD) usually develops in patients with an individual or family history of allergic diseases, and is characterized by chronic relapsing inflammation seen especially in childhood, association with IgE hyperproduction and precipitation by environmental factors. However, the exact etiology of AD has been unclear. To further explore the pathogenesis and treatment of AD, a suitable animal model is required. We found that skin lesions, which were clinically and histologically very similar to human AD, spontaneously appeared on the face, neck, ears and dorsal skin of inbred NC/Nga mice when they were raised in non-sterile (conventional) circumstances, but not under specific pathogen-free conditions. Plasma levels of total IgE in conventional NC/Nga mice were markedly elevated from 8 weeks of age, correlating with clinical skin severity of dermatitis. Immunohistochemical examination of the skin lesion showed increased numbers of mast cells and CD4+ T cells containing IL-4 necessary for IgE synthesis. Thus, NC/Nga mice suffered from dermatitis very similar to human AD with IgE hyperproduction, which may be triggered by some environmental factor(s).
authors.affiliation: Department of Veterinary Clinic, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Matsuda
authors.forename: N
authors.initials: N
authors.lastname: Watanabe
authors.forename: G P
authors.initials: GP
authors.lastname: Geba
authors.forename: J
authors.initials: J
authors.lastname: Sperl
authors.forename: M
authors.initials: M
authors.lastname: Tsudzuki
authors.forename: J
authors.initials: J
authors.lastname: Hiroi
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Ushio
authors.forename: S
authors.initials: S
authors.lastname: Saito
authors.forename: P W
authors.initials: PW
authors.lastname: Askenase
authors.forename: C
authors.initials: C
authors.lastname: Ra
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000097:blood / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D006942:Hypergammaglobulinemia / Q000097:blood / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D007073:Immunoglobulin E / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D008407:Mast Cells / Q000276:immunology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008815:Mice, Inbred Strains / Q000097:blood / Q000235:genetics / Q000276:immunology*; D008817:Mice, Mutant Strains; D013047:Specific Pathogen-Free Organisms
chemical_list: D007073:Immunoglobulin E