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• W2064622633 endingPage "869" @default.
• W2064622633 startingPage "845" @default.
• W2064622633 abstract "At least 20 years have passed since the pathogenesis of asthma and allergic rhinitis formally was attributed to immunoglobulin E (IgE)-dependent mechanisms. Since then, the concept that upper and lower airway inflammation leads to chronic airway disease widened the search for the types of cellular and molecular interactions that are responsible for linking the initial stimulus to the final abnormality in airway function. It has not been possible to integrate this information into a single model for the development of airway inflammation and remodeling, but a useful framework has been based on the behavior of the adaptive immune system. In that paradigm, an exaggeration of T helper type 2 (TH2) over TH1 responses to allergic and nonallergic stimuli leads to airway inflammatory disease, especially asthma. This article examines the role of antigen-presenting cells in the TH2 bias in allergic rhinitis (an upper airway disease) and how this process differs in asthma (a lower airway disease). Alternative evidence is summarized that implicates a principal component of the innate immune response (ie, airway epithelial cells) in the pathogenesis of asthma. This new model highlights specific interactions between epithelial, viral, and allergic (Epi-Vir-All) components and better explains the basis for airway immunity, inflammation, and remodeling in response to viral infection. The development of long-term disease phenotypes that are typical of asthma and other hypersecretory airway diseases, which include allergic rhinitis, can be understood more clearly using this model." @default.
• W2064622633 created "2016-06-24" @default.
• W2064622633 creator A5036584012 @default.
• W2064622633 creator A5043556111 @default.
• W2064622633 date "2002-11-01" @default.
• W2064622633 modified "2023-10-18" @default.
• W2064622633 title "Lessons from allergic rhinitis versus asthma pathogenesis and treatment" @default.
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