Harvey's Garden

Type I hypersensitivity reaction

1 min read

Etiology

Pathophysiology

  • 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

  • Early (Immediate) Phase (minutes)
    • Release of preformed mediators from granules.
    • Histamine: Vasodilation, ↑ vascular permeability (wheal), bronchoconstriction, mucus production.
    • Tryptase: Mast cell-specific marker; can be measured in serum to confirm anaphylaxis.
  • Late Phase (hours)
    • Synthesis of new mediators.
    • Leukotrienes (C4, D4, E4): Potent bronchoconstrictors, ↑ vascular permeability. More potent and longer-lasting than histamine.
    • Prostaglandins (esp. D2): Vasodilation, bronchoconstriction.
    • Cytokines (e.g., TNF-α, IL-5): Recruit and activate other inflammatory cells.
      • IL-5 is the key chemotactic factor for eosinophils.
      • Eosinophils are recruited and release their granule contents, including Major Basic Protein (MBP), which is cytotoxic to epithelial cells and contributes to the chronic tissue damage seen in conditions like asthma.

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.

Treatment

Graph View

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