The problem of contact allergic dermatitis in humans and contact hypersensitivity in animals begins with the observation that certain reactive compounds, when placed on skin, lead to a reproducible and characteristic inflammatory reaction. The immunologic processes that conspire to produce this damaging tissue reaction are derived from the normal immunologic balance between the protection of self and the destruction of nonself. Experimental work in the last decade has focused on the role of antigen-presenting cells, and specifically Langerhans cells, in the initiation of contact hypersensitivity, as well as on the competing roles of subsets of T lymphocytes in its regulation. For humans, an important goal has been the development of techniques by which tolerization and desensitization may be achieved, and for those who work with laboratory animals, contact hypersensitivity has provided methods to examine immune regulation in general. In the coming decade, we anticipate that new echniques from molecular biology, molecular genetics, tissue culture, and, above all, shrewd clinical observation will provide a new array of ideas and possibilities.
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