Type I hypersensitivity reaction pathway

Type I hypersensitivity reaction pathway, also known as the immediate or IgE-mediated hypersensitivity pathway, is not a single molecular target or receptor but a multi-step cellular and molecular cascade vital to the pathogenesis of allergic diseases and anaphylaxis. It begins with sensitization, where exposure to allergen induces allergen-specific IgE production by B cells (with T-helper 2 cell help). IgE binds to high-affinity FcεRI receptors on mast cells and basophils. Upon re-exposure, allergen cross-links surface-bound IgE, triggering rapid degranulation and release of preformed (e.g., histamine, tryptase) and newly synthesized mediators (e.g., leukotrienes, prostaglandins), which cause vascular leak, smooth muscle contraction, mucus secretion, and inflammation. The late phase involves recruitment of eosinophils and other leukocytes, contributing to chronic allergic pathology. This pathway underlies conditions such as anaphylaxis, allergic rhinitis, asthma, atopic dermatitis, and food allergies[1][3][4][5]. Note: "Type I hypersensitivity reaction pathway" refers to a biological process, not to a discrete, druggable molecular target or receptor. It is a pathway comprising several cellular and molecular players (IgE, FcεRI, mast cells, mediators, etc.), none of which is specifically called the "Type I hypersensitivity reaction pathway." It is thus not considered a single therapeutic target but rather a process targeted at multiple points (e.g., IgE, FcεRI, mediators)[1][3][4].

Other names

Immediate hypersensitivity reaction pathwayIgE-mediated hypersensitivity pathwayAllergic reaction pathwayAnaphylactic pathway

Blockade of histamine receptors (antihistamines), Inhibition of mast cell degranulation (omalizumab), Reduction of inflammation (corticosteroids), Counteraction of anaphylaxis via vasoconstriction and bronchodilation (epinephrine), Blockade of leukotriene receptors