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Immunoglobulin E (IgE) is a class of antibody produced by B cells in response to allergens and certain parasitic infections[2]. IgE binds with high affinity to the Fc epsilon receptor I (FcεRI), which is highly expressed on the surface of mast cells and basophils[2]. Crosslinking of FcεRI-bound IgE by antigen leads to cellular activation, degranulation, and release of mediators such as histamine, proteases, cytokines, and lipid mediators, causing immediate hypersensitivity reactions and inflammation[1][2][4]. This complex also contributes to the survival, proliferation, and homeostasis of mast cells in inflamed tissues[1]. Therapeutics targeting IgE or FcεRI, such as omalizumab, prevent IgE-mediated cell activation and are effective for severe allergic and inflammatory disease. The target as commonly phrased (“IgE antibodies on the surface of mast cells and basophils”) is technically imprecise; the actionable molecular target is either IgE itself, FcεRI, or the IgE-FcεRI complex[2][4].
IgE-neutralizing antibodies (e.g., omalizumab) bind circulating IgE, preventing its interaction with FcεRI, leading to downregulation of receptor and decreased cell activation. FcεRI antagonists prevent IgE binding or crosslinking. Drugs may reduce release of mediators (e.g., histamine, cytokines, leukotrienes) by inhibiting cell activation.
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