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North American Airway Collaborative (NoAAC) model of proximal airway disease pathogenesis. Epithelial dysfunction facilitates displacement of antigenic triggers across the mucosal barrier. Inappropriate host immune responses drive inflammation resulting in pathologic fibroblast activation and subsequent extracellular matrix deposition. Genetics and estrogen may each influence barrier function, immune activation, or fibroblast phenotype in the proximal airway mucosa.
