Exposure to inhaled allergens, such as pollen can initiate an acute immune response in allergen-sensitive individuals that leads to airway inflammation. Persistent inflammation is associated with allergen-induced asthma, a chronic respiratory disorder characterized by the production of IgE antibodies, airway hypersensitivity, and thickening of the airway wall. Allergens are initially processed by dendritic cells which promote naïve T cells to differentiate into T helper type 2 cells (Th2). These Th2 cells produce cytokines, including IL-4 and IL-13 that, along with specific co-stimulatory molecules, induce B cells to produce allergen-specific IgE antibodies. IgE antibodies bind with high affinity to the Fc epsilon RI receptors found on mast cells, basophils, neutrophils, and eosinophils. Upon allergen re-exposure, allergen binding to IgE-Fc epsilon RI receptors on mast cells and basophils promotes receptor cross-linking and triggers the release of pro-inflammatory mediators, such as histamine and cysteinyl leukotrienes, that define the early phase asthmatic reaction. The late phase asthmatic reaction occurs several hours after the initial reaction and is characterized by eosinophil activation and leukocyte recruitment to the sites of allergen exposure. The release of cytokines and chemokines at these sites by infiltrating leukocytes plays a critical role in promoting chronic inflammation and airway remodeling. R&D Systems offers a wide variety of research reagents useful for the characterization of allergen-induced immune response pathways.