Inflammatory patterns in allergic rhinitis

Summary Allergic rhinitis results from allergen‐triggered early and late responses that are mediated by an array of inflammatory cells and mediators. Exposure to allergen induces the proliferation of T‐helper type 2 (Th2) lymphocytes in allergic individuals leading to the subsequent release of a characteristic combination of cytokines that promotes IgE and mast cell production. Within the allergic epithelium, there is proliferation of mucosal mast cells that express IL‐4, IL‐5, IL‐6 and tryptase. The resultant inflammatory mediators and cytokines enhance endothelial expression of adhesion molecules, such as vascular cell adhesion molecule‐1. Chemoattractants, such as eotaxin, RANTES and IL‐5, are responsible for the characteristic infiltration of the nasal mucosa by eosinophils, basophils, mast cells and Th2 lymphocytes that is seen in the late‐phase allergic response.