Abstract
A wide body of epidemiologic evidence indicates that in children at high genetic risk of allergic diseases, programming of TH2-polarized immunologic memory associated with progressively increasing IgE antibody production is most commonly initiated during the preschool years (reviewed in Holt et al1 and Holt and Thomas2), and there is growing interest in “early intervention” aimed at arresting this process before it becomes persistent. The basis for one emerging therapeutic strategy is the consistent finding in experimental models that development of resistance to inhalant allergy is actively driven by environmental allergen exposure via the nasopharyngeal mucosa, resulting in the induction of a form of immunologic tolerance mediated by regulatory T cells, which target allergen-specific TH2 memory cells (reviewed in Strickland et al3).
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