Repeated inhalation of allergen leads to the downregulation of allergen-specific IgE responses in non-atopic individuals as well as in mice. This phenomenon is named as inhalation- induced IgE tolerance. In contrast, inhaled allergen causes significant IgE and allergic responses in atopic persons. The mechanisms involved in this differential regulation of airway allergen-specific immune responses remain unclear. Besides the allergen exposure in genetic susceptible individuals, environmental contaminant is considered to play as an initiating factor for airway allergic responses. By using murine model, we demonstrate here that airborne b-1,3- glucan, which exists frequently in our environments particularly in highly humid area, can abrogate inhalation- induced IgE isotype-specific down- regulation and promote airway eosinophil infiltration to inhaled antigen
