Type I hypersensitivity reaction

Etiology

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.

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.

Tryptase
- A relatively specific marker of mast cell activation
- Elevated levels indicate an increased risk of severe reactions.