Potential role of environmental factors in the etiology and pathogenesis of atopy: A working model

Abstract

Sensitization to inhalant allergens commonly commences in utero, and most children are born with weak T helper-2 (Th2)-polarized T-cell immunity to these agents. During early life, these responses are normally deviated toward the Th1 cytokine profile. However, in atopics this immune deviation process fails, leading instead to consolidation of allergen-specific Th2 immunity and its eventual active expression in the airways. Both the induction and expression of Th2 immunity can be modulated by environmental agents that affect the cytokine milieu in the airway mucosa and/or the draining lymph nodes. Because of the known effects of the mold cell wall component (1→3)-β-D-glucan on monocyte cytokine secretion, exposure to molds during childhood may be a significant etiologic factor in allergic respiratory disease in general.