Allergic airway inflammation is one characteristic feature of asthma disease, with additional pathology including a reversible airway obstruction, airway hyperresponsiveness (AHR), infiltration of eosinophils and T-helper type 2 (Th2) cells into the airway submucosa, mucus hypersecretion, and airway remodeling (Agrawal & Shao 2010). Allergic airway diseases are inflammatory disorders in which aberrant immune regulation occurs and susceptible individuals mount allergen specific responses. Inflammatory cells are recruited to the asthmatic airways or are activated in situ. The inflammatory cells include mast cells, macrophages, eosinophils, T lymphocytes, dendritic cells, basophils, neutrophils, and platelets (Barnes et al. 1998). Structural cells may also be important sources of inflammatory mediators in asthma. Airway epithelial cells, smooth muscle cells, endothelial cells, and fibroblasts are all capable of synthesizing and releasing inflammatory mediators (Levine, 1995; Saunders et al. 1997; John et al. 1997). Moreover, these cells may become the major source of inflammatory mediators in the airway, which may explain how asthmatic inflammation persists even in the absence of activating stimuli. A majority of patients with asthma have an atopic, allergic background (Robinson 2000). The prevailing consensus in regards to these patients is that the immunological basis of atopic sensitization and allergic disease results from inappropriate Th2 cell responses to common environmental proteins termed allergens (Robinson 2009). Here, we summarize recent findings regarding how immune response and inflammatory cells contribute to allergic airway inflammation and discuss recent progress in the regulation of these cells.