In Type I (immediate/anaphylactic) hypersensitivity, on re-exposure to allergen, cross-linking of IgE bound to FcεRI receptors on mast cells and basophils triggers degranulation, releasing both preformed (primary) mediators stored in granules and newly synthesized (secondary) mediators.
Primary (preformed) mediators — stored within cytoplasmic granules and released immediately on degranulation:
Histamine — the principal preformed mediator; causes vasodilation, increased vascular permeability, smooth muscle contraction (bronchospasm, gut spasm), and increased mucus secretion; acts on H1 receptors for these effects.
Tryptase and chymase — proteolytic enzymes; tryptase is used clinically as a serum marker to confirm mast cell degranulation (e.g., in suspected anaphylaxis).
Heparin — an anticoagulant proteoglycan, also helps package/store the other granule contents.
Eosinophil chemotactic factor of anaphylaxis (ECF-A) and neutrophil chemotactic factor — recruit eosinophils/neutrophils, contributing to the later-phase response.
These preformed mediators account for the immediate reaction (within minutes), producing the classical features of urticaria, bronchospasm, and (in severe cases) anaphylactic shock; newly synthesized mediators (leukotrienes, prostaglandin D2, platelet-activating factor — derived from arachidonic acid metabolism of the mast cell membrane) and recruited inflammatory cells drive the late-phase reaction occurring several hours later.
