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Richard A. F. Clark, MD

Arch Dermatol. 1989;125(3):413-416.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 ingestion^2-5 and aeroallergen contact^6-11 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 . . . [Full Text PDF of this Article]

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

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