Abstract
Sensitization, as proven by the demonstration of low levels of immunoglobin E (IgE) antibodies directed against environmental allergens, appears to be part of the normal immune response (1). In most instances these antibodies are only temporary, as the continuing IgE antibody formation is rapidly suppressed. But when genetically predisposed individuals are exposed to an allergen at a time when the regulation of the immune system is immature, then higher levels of IgE antilbodies, lasting for a long time, may appear. The more susceptible to sensitization the individual is, the lower is the allergen dose needed for this to occur. The fact that an individual is sensitized does not, however, necessarily mean that clinical symptoms, i.e., allergic disease, will develop. It is not known which factors decide what allergic manifestations will appear in an atopic individual, e.g., whether he or she will suffer from atopic dermatitis, asthma, hay fever, gastrointestinal allergy, or several of them. It is likely, however, that the selection of a target organ is also at least partially under genetic control.
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Björkstén, B. (1998). Ontogeny of Allergy. In: Denburg, J.A. (eds) Allergy and Allergic Diseases. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4757-2776-0_4
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