The Direct and Indirect Role of IgE on Airway Epithelium in Asthma

Asthma is a chronic airway inflammatory disorder, affecting over 350 million people worldwide, with allergic asthma being the most common form of the disease. Allergic asthma is characterized by a type 2 (T2) inflammatory response triggered by numerous allergens beginning in the airway epithelium, which acts as a physical barrier to allergens as well as other external irritants including infectious agents, and atmospheric pollutants. T2 inflammation is propagated by several key cell types including T helper 2 (Th2) cells, eosinophils, mast cells, and B cells. Immunoglobulin E (IgE), produced by B cells, is a key molecule in allergic airway disease and plays an important role in T2 inflammation, as well as being central to remodeling processes within the airway epithelium. Blocking IgE with omalizumab has been shown to be efficacious in treating allergic asthma however, the role of IgE on airway epithelial cells is less communicated. Developing a deeper explanation of the complex network of interactions between IgE and the airway epithelium will facilitate an improved understanding of asthma pathophysiology. This review discusses the indirect and direct roles of IgE on airway epithelial cells, with a focus on allergic asthma disease.