Recent evidence suggests that the development of chronic allergic respiratory disease is a biphasic process. Phase 1 commonly occurs during early childhood and in many instances appears to be initiated in utero. This involves initial priming of the Th-cell system against ubiquitous environmental allergens, and subsequent reshaping of these responses during infancy into Th1- or Th2-polarized immunological memory. The second phase of the process comprises the repeated expression of Th2-polarized allergen-specific immunity at the level of the airway mucosa, producing cumulative damage to local tissue resulting ultimately in phenotypic changes including development of airways hyperreactivity. It is also clear that this second phase occurs in only a relatively small subset of subjects who develop long-term Th2-polarized allergen-specific immunity, given that the majority of skin prick test positive subjects do not develop chronic airways disease. This suggests that an additional set of control mechanisms, which regulate the intensity/duration of local Th-cell responses within airway mucosal tissues, may play an important role in the ultimate expression of chronic immunoinflammatory disease in the airways in ‘at risk’ atopic subjects.
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