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March 1989

Cell-Mediated and IgE-Mediated Immune Responses in Atopic Dermatitis

Author Affiliations

National Jewish Center for Immunology and Respiratory Medicine 1400 Jackson St Denver, CO 80206

Arch Dermatol. 1989;125(3):413-416. doi:10.1001/archderm.1989.01670150103018

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.1 Recently, food ingestion2-5 and aeroallergen contact6-11 have 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.12-21 Yet, 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 Sulzberger22 reported 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,23-27 while others found that contact sensitization with haptenic chemicals such as nickel sulfate, potassium

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