THE MECHANISMS AND EVALUATION OF CHEMICALLY-INDUCED ALLERGY

Many chemicals are able to induce contact allergy, a delayed-type hypersensitivity reaction. Some of these have, in addition, the potential to cause respiratory allergy, an immediate hypersensitivity reaction effected by IgE antibody. The characteristics of immune responses provoked by chemical allergens determine the type of hypersensitivity reaction which will predominate. Recent evidence indicates that contact and respiratory allergens stimulate qualitatively different immune responses in mice consistent with the selective activation of T helper (T(H)) cell subpopulations. Contact allergens which lack the potential for respiratory sensitization preferentially activate T(H1) cells which effect delayed-type hypersensitivity reactions. A soluble product of T(H1) cells, interferon gamma (IFN-gamma), inhibits IgE antibody responses, and thereby the induction of respiratory sensitization. Conversely, chemical allergens which are known to cause respiratory hypersensitivity stimulate preferentially T(H2)-type responses. T(H2) cells promote the development of respiratory allergy through the production of interleukin 4 (IL-4), a cytokine which is required for the initiation and maintenance of IgE responses. Although the molecular basis for the selective activation by contact and respiratory allergens of T(H1) and T(H2) cells, respectively, awaits clarification, these qualitative differences in immune response provide opportunities for the identification and evaluation of chemical sensitizers.