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 (TH) cell subpopulations. Contact
allergens which lack the potential for respiratory sensitization preferentially activate TH1 cells which effect delayed-type
hypersensitivity reactions. A soluble product of TH1 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 TH2-type responses. TH2 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 TH1 and TH2 cells, respectively, awaits clarification, these qualitative differences in immune response provide opportunities for the identification and evaluation of chemical sensitizers.