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Article
October 1991

Recent Developments in the Pathogenesis of Allergic Contact Dermatitis

Author Affiliations

From the Department of Dermatology, University of Minnesota, Minneapolis. Dr Kalish is now with the Department of Dermatology, Health Sciences Center, State University of New York at Stony Brook.

Arch Dermatol. 1991;127(10):1558-1563. doi:10.1001/archderm.1991.01680090122016
Abstract

• Allergic contact dermatitis is both an important clinical problem and a model system for lymphocyte-mediated pathologic changes. Elicitation of allergic contact dermatitis requires interaction of antigen with epidermal Langerhans cells, followed by migration of the Langerhans cells to the lymph nodes to present antigen to T lymphocytes. These activated T lymphocytes must then home to the antigen-exposed skin. Adhesion molecules such as LFA-1 and ICAM-1 have a role in this homing. Only a small proportion of the T lymphocytes in the skin lesion are specific for the inducing antigen. Studies of poison ivy (urushiol dermatitis) have determined this fraction to be less than one per 100 infiltrating lymphocytes. By a variety of amplification mechanisms, it is possible for this small number of antigen-specific T lymphocytes to induce the pathologic changes of allergic contact dermatitis. Improved understanding of this condition should result in increased knowledge of the pathogenesis of a variety of T lymphocyte—mediated skin conditions.

(Arch Dermatol. 1991;127:1558-1563)

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