IgE-driven kind I hypersensitivity reactions are characterised by an exaggerated immune response to usually innocent environmental substances, corresponding to pollen, mud mites, or meals proteins.1 The severity of such allergic reactions can manifest with signs starting from average native irritations (ie, rhinoconjunctivitis) to deadly multiorgan failure (ie, anaphylaxis). Binding of allergen-specific IgE to its high-affinity IgE receptor, FcεRI, on mast cells (MCs) and basophils is on the core of the allergic pathophysiology, as allergen-mediated cross-linking of FCεRI-bound IgE triggers an intracellular signaling cascade in these cells ensuing within the launch of prestored and de novo synthesized inflammatory mediators (ie, histamine, leukotrienes, prostaglandins, cytokines, chemokines, and proteases).
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