IgEdependent

IgE-dependent refers to immune processes that require immunoglobulin E (IgE) as a central mediator. IgE is produced by plasma cells in response to signals from a T helper 2 (Th2)–skewed immune response. In sensitized individuals, IgE binds with high affinity to FcεRI receptors on the surface of mast cells and basophils, establishing a state of sensitization.

Upon subsequent exposure to the same allergen, the allergen cross-links the bound IgE on these cells, triggering degranulation and the release of mediators such as histamine, prostaglandins, and leukotrienes. This rapid mediator release causes symptoms of immediate-type hypersensitivity, including vasodilation, increased vascular permeability, smooth muscle contraction, and mucus production.

IgE-mediated reactions underpin many allergic diseases, such as allergic rhinitis, conjunctivitis, allergic asthma, and anaphylaxis. Diagnosis relies on patient history plus tests for IgE sensitization, including skin prick tests and measurement of serum allergen-specific IgE.

Management emphasizes avoidance of known allergens, pharmacotherapy (antihistamines, intranasal corticosteroids, inhaled bronchodilators and corticosteroids), and emergency treatment for anaphylaxis. Biological therapies that reduce IgE levels or block its interaction with FcεRI, notably omalizumab, are used in selected patients. Beyond allergy, IgE contributes to defense against parasitic helminths, though in many modern settings IgE sensitization can contribute to pathology rather than protection.