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• W2032068275 abstract "Although the pathogenesis of atopic dermatitis is unknown, abundant scientific evidence suggests that immunologic mechanisms contribute to the development of atopic dermatitis in many patients.¹Recently, food ingestion^2-5and aeroallergen contact^6-11have been shown to initiate flares of atopic dermatitis. Immediate and late-phase reactions of IgE-mediated immunity and/or delayed hypersensitivity reactions of cell-mediated immunity have been postulated as pathophysiologic processes by which these antigen-provoked flares of atopic dermatitis may occur.^12-21Yet, many reports in the literature have claimed that the cell-mediated type of delayed hypersensitivity is suppressed in atopic dermatitis.^22-41 As evidence for suppression of cell-mediated immunity, Rostenberg and Sulzberger²²reported a low incidence of contact dermatitis to haptenic chemicals such as nickel sulfate, potassium dichromate, and balsam of Peru in patients with atopic dermatitis. Later, some investigators confirmed these observations,^23-27while others found that contact sensitization with haptenic chemicals such as nickel sulfate, potassium" @default.
• W2032068275 created "2016-06-24" @default.
• W2032068275 creator A5076772705 @default.
• W2032068275 date "1989-03-01" @default.
• W2032068275 modified "2023-09-26" @default.
• W2032068275 title "Cell-Mediated and IgE-Mediated Immune Responses in Atopic Dermatitis" @default.
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• W2032068275 doi "https://doi.org/10.1001/archderm.1989.01670150103018" @default.
• W2032068275 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/2647030" @default.
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