IL4 and airway hyperresponsiveness: IL-4 activates B cells to differentiate into plasma cells that generate immunoglobulin E (IgE) required for mast cell responses to allergens; IL-5 promotes eosinophil differentiation and survival; IL-13, IL-4, and other inflammatory mediators promote goblet cell overexpression, increased mucus secretion, as well as airway hyperresponsiveness, then contributing to the hallmarks of asthma pathophysiology (7, 11–13).