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High-affinity immunoglobulin E receptor (**FcεRI**) is a cell-surface receptor found on mast cells and basophils. When allergen-specific IgE antibodies bind FcεRI and are subsequently cross-linked by allergen, this triggers rapid degranulation of mast cells/basophils, releasing preformed mediators—most notably **histamine**—that lead to the immediate symptoms of allergy, including itching, swelling, bronchoconstriction, and potentially life-threatening anaphylaxis[2][3][4][5]. This process is fundamental to the pathology of allergic diseases and is a validated target for treatment using biologics such as omalizumab and other anti-IgE therapies[2][4]. Drugs targeting FcεRI/IgE can reduce allergic inflammation and prevent hypersensitivity reactions by blocking the activation pathway.
Blockade of IgE binding to FcεRI (e.g., omalizumab prevents IgE from activating the receptor); Inhibition of histamine release via blockade of mast cell activation; Downregulation of FcεRI expression (via reduced serum IgE)
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