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The **high-affinity immunoglobulin E receptor (FcεRI)** is a multimeric cell surface receptor expressed predominantly on mast cells and basophils; it binds IgE with high affinity and mediates activation of these cells during allergic responses[2][4]. Crosslinking of FcεRI-bound IgE by allergens triggers degranulation and secretion of inflammatory mediators like histamine, cytokines (IL-4, IL-13), and lipid mediators, leading to the symptoms of immediate hypersensitivity (allergic reactions)[1][2][3][4]. FcεRI is a key therapeutic target in allergic and some autoimmune diseases, with several drugs designed to block IgE binding or downstream signaling. Notably, the presence of IgE itself enhances FcεRI levels and mast cell survival, making both molecules central to type I hypersensitivity and chronic allergic inflammation[1][2].
Inhibition of IgE binding to FcεRI to prevent cell activation and degranulation[1][4] - Downregulation of FcεRI expression via IgE sequestration[1]
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