ABSTRACT
Rocklin et al. have demonstrated not only the existence of antigen-specific suppressor cells for ragweed antigen E in humans, but have also shown that this suppression is increased by allergy desensitization in perhaps the first demonstration of immunotherapy through suppressor function. If this type of suppression can be mediated by a genetically nonrestricted soluble factor the potential would be quite impressive. It may be necessary to develop different tools and models to look at suppressor function in allergy than have already been used in autoimmunity. Allergy can result from an intrinsic B cell defect resulting in reagenic antibody synthesis regardless of immunoregulatory milieu, helper T cell excess inducing IgE synthesis or a suppressor T cell defect allowing IgE synthesis in a situation not optimal for the organism at that time. Humans with atopic disease have elevated total IgE levels and produce IgE antibodies to allergens to which they are sensitive in much greater quantity than do normals.
