An airbone mold-derived product, -1,3-D-glucan, potentiates airway allergic responses
Wan, G., Li, C.S. Guo, S.P. Rylander, R. adn Lin, R.H.
1999 European Journal of Immunology,
Wan, G., Li, C.S. Guo, S.P. Rylander, R. adn Lin, R.H., (1999), "An airbone mold-derived product, -1,3-D-glucan, potentiates airway allergic responses", European Journal of Immunology,.
Abstract:
Repeated inhalation of allergen leads to the down-regulation of allergen-specific IgE responses in non-atopic individuals as well as in mice. This phenomenon is named 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 of genetically susceptible individuals, environmental contamination is considered to play a role as an initiating factor for airway allergic responses. Using a murine model, we demonstrate here that airborne -1,3-D-glucan, which exists frequently in our environment, particularly in highly humid areas, can abrogate inhalation-induced IgE isotype-specific down-regulation and promote airway eosinophil infiltration to inhaled antigen.
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