[Pathogenesis and guidelines for therapy of atopic dermatitis].
Atopic dermatitis (AD) is regarded as one of type 2 helper T cell (Th2)-mediated diseases. However, our data by in situ hybridization elucidated mRNA expressions of both Th1 and Th2 cyotokine in the lesions of AD. Some work revealed a decrease of Th1 mRNA without a change of Th2 mRNA after remission by therapy. Th1 may closely relate to skin lesions of AD. Our work showed a IL-4 and IL-5 production and a elevated expression of high affinity IgE receptor by eosinophils in the lesions of AD. Uptake of allergens may be mediated by the receptor and may lead to a release of cytokines. A guideline for therapy for AD, supported by a Ministry of Health and Welfare in Japan, is published in 1999. In this paper, the guideline was outlined.
Tanaka
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Y
Department of Dermatology, National Kawatana Hospital.
D000818:Animals; D016207:Cytokines / Q000096:biosynthesis; D003876:Dermatitis, Atopic / Q000209:etiology* / Q000473:pathology / Q000628:therapy*; D019983:Guideline Adherence; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D008925:Mites / Q000276:immunology; D012333:RNA, Messenger / Q000096:biosynthesis; D017455:Receptors, IgE / Q000096:biosynthesis
D016207:Cytokines; D012333:RNA, Messenger; D017455:Receptors, IgE; D015847:Interleukin-4; D007371:Interferon-gamma