IgE is the less abundant immunoglobulin isotype in serum and displays higher affinity for its cognate Fc receptor (FceRI) than the rest of antibody isotypes. Moreover, the class switch recombination and the generation of memory responses remarkably differ between IgE and other isotypes. Importantly, class switch recombination to IgE can occur in the mucosae, preferentially through the sequential switching from IgG. Therefore, resident effector cells get rapidly sensitized, and free IgE can be found in mucosal secretions. All these aspects explain the involvement of IgE in respiratory diseases. In allergic rhinitis and allergic asthma, the IgE-sensitization to environmental allergens triggers an eosinophilic inflammation of the airway mucosa of atopic patients. In recent years, growing evidence indicates that some non-atopic patients with nasal reactivity to allergens display nasal eosinophilic inflammation, which could be triggered by the local production of allergen-specific IgE. This phenotype has been termed local allergic rhinitis. Mucosal IgE is also implicated in the pathophysiology of chronic rhinosinusitis with nasal polyps, even though the mechanisms for IgE synthesis might differ in this case. The role of IgE as mediator of airway diseases identify this marker as a therapeutic target. Some biologicals antagonize IgE-mediated inflammation of the airway mucosa, but they have not shown a beneficial long-term effect after discontinuation. In contrast, allergen immunotherapy does not only control the symptoms of airway allergy, but it also induces a long-lasting effect after discontinuation, thus modifying the natural course of the disease.
