When a multivalent antigen comes in contact with the cell, multiple IgE antibodies become cross-linked, resulting in aggregation of the FcεRI receptors on the mast cell surface.
This clumping of receptors leads to the activation of non-receptor tyrosine kinases, triggering an intracellular cascade that ultimately results in mast cell and basophil degranulation.
Timing
After first exposure to an allergen (eg, peanuts), antigen specific IgE is produced by B-cells and binds to the surface of mast cells. If repeat exposure occurs, the bound IgE can cross-link and stimulate the release of preformed histamine and leukotrienes that cause vasodilation and increased capillary permeability. The result is a rapid (eg, minutes after exposure) early-phase type I hypersensitivity response characterized by superficial dermal edema and erythema (eg, wheal and flare reaction) that can progress to a more systemic response (eg, anaphylaxis).
IgE also initiates the late phase of a type I hypersensitivity reaction by stimulating type 2 helper T cells to release cytokines (eg, IL-5) that activate eosinophils. Cationic proteins (eg, major basic protein, eosinophil peroxidase) released from eosinophils cause tissue damage, which usually manifests as a palpable, indurated lesion 2-10 hours following the early-phase reaction.
Clinical features
Diagnostics
Hypersensitivity blood tests (in vitro)
Tryptase
A relatively specific marker of mast cell activation
Elevated levels indicate an increased risk of severe reactions.
