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IgE-mediated (atopic) allergy depends on the production of IgE antibodies to normally harmless substances. It is associated with other immunological abnormalities, particularly defects in the T lymphocyte system, and is now generally considered to be a manifestation of IgE-suppressive immunodeficiency. Experiments with adult laboratory animals have revealed the existence of an IgE-selective immunoregulatory system and great efforts are being made to understand the mechanisms by which this system operates, to compensate for, or correct, the deficiency of atopic individuals. However, since allergy is often a problem of childhood one might reasonably ask if experiments with adult animals are a wholly appropriate approach to the problem. Rats were used to explore factors influencing the development of IgE regulation during early life, when the immunological apparatus differs intrinsically from that of mature animals. The results of these experiments, which have shown profound IgE-suppressive effects of maternal antibody and of neonatally ingested antigen, are reviewed with the aim of stimulating research on this topic in man.

The development of immediate hypersensitivities depends essentially on the production of IgE antibodies--usually to common environmental antigens. It has been suggested that atopic individuals produce IgE antibodies as a result of overstimulation with antigen and that this occurs through IgA deficiency which by default allows the absorption via the mucosae of abnormally large amounts of antigen. However, work with laboratory animals indicates a mechanism which is the antithesis of the overstimulation concept: that quantities of antigen sufficiently large to activate IgE immunoregulatory mechanisms, particularly suppressor T cells, are normally absorbed across the mucosae and that, where other conditions for the activation of these cells are appropriate, inhibition rather than stimulation of IgE responses results. In this way allergies arise through a defect of one or more components of the immunoregulatory mechanism. The fact that atopic individuals do not become allergic to all ubiquitous antigens and that they may be hyposensitised is evidence that the defect is relative rather than absolute.