title: Conversion of the CD4+ T cell profile from T(H2)-dominant type to T(H1)-dominant type after varicella-zoster virus infection in atopic dermatitis.
abstract: Skin lesions of atopic dermatitis were examined for cytokine expression by reverse transcription-polymerase chain reaction. The profile of mRNA for various cytokines revealed that both T(H1) and T(H2) types of CD4+ T cells, probably including T(H0) type, infiltrate into the skin lesion. We observed that atopic skin lesions improved after varicella infection. In such lesions, expression of T(H1) type cytokines predominated. The peripheral blood T cells from atopic patients exhibited a differentiation into T(H2) type cells upon in vitro stimulation with mite antigen. In contrast they differentiated into T(H1) type cells upon stimulation by varicella antigen. Since IL-12 has been reported to switch the in vitro recall response of allergen-specific T cells of atopic donors from a T(H2)- to a T(H1)-like phenotype, we examined its local production in varicella lesions. IL-12 p35 and p40 mRNA were expressed in fresh lesions. Peripheral blood mononuclear cells from atopic patients expressed p40 mRNA upon in vitro stimulation with live varicella zoster virus, but they did not show p40 mRNA without stimulation. This finding suggested that in atopic skin lesions containing the virus, IL-12 was produced and the cell type was changed to T(H1) type-predominance. These results suggested that patients with atopic dermatitis always have highly reactive CD4+ T cells infiltrating into their skin, and that the switch to T(H1) or T(H2) dominance is related to whether the lesion is improved or exacerbated.
authors.affiliation: Department of Dermatology, Kitasato University School of Medicine, Kanagawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Fujimura
authors.forename: R
authors.initials: R
authors.lastname: Yamanashi
authors.forename: M
authors.initials: M
authors.lastname: Masuzawa
authors.forename: Y
authors.initials: Y
authors.lastname: Fujita
authors.forename: K
authors.initials: K
authors.lastname: Katsuoka
authors.forename: S
authors.initials: S
authors.lastname: Nishiyama
authors.forename: M
authors.initials: M
authors.lastname: Mitsuyama
authors.forename: K
authors.initials: K
authors.lastname: Nomoto
mesh_terms: D000956:Antigens, Viral / Q000494:pharmacology; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D004797:Enzyme-Linked Immunosorbent Assay; D006562:Herpes Zoster / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D014645:Herpesvirus 3, Human / Q000276:immunology; D006801:Humans; D018664:Interleukin-12 / Q000096:biosynthesis; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000956:Antigens, Viral; D016207:Cytokines; D012333:RNA, Messenger; D018664:Interleukin-12