Activation of IgE regulatory mechanisms by transmucosal absorption of antigen.
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.
D000042:Absorption; D000818:Animals; D000917:Antibody Formation; D001666:Binding Sites, Antibody; D004406:Dysgammaglobulinemia / Q000150:complications / Q000276:immunology; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000209:etiology*; D007071:Immunoglobulin A, Secretory; D007073:Immunoglobulin E / Q000096:biosynthesis*; D051379:Mice; D009092:Mucous Membrane / Q000276:immunology; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology
D007071:Immunoglobulin A, Secretory; D007073:Immunoglobulin E