Type I Hypersensitivity - Pathophysiology

Pathophysiology

In type 1 hypersensitivity, an antigen is presented to CD4+ Th2 cells specific to the antigen that stimulate B-cell production of IgE antibodies also specific to the antigen. The difference between a normal infectious immune response and a type 1 hypersensitivity response is that in type 1 hypersensitivity the antibody is IgE instead of IgA, IgG, or IgM. During sensitisation, the IgE antibodies bind to Fcε receptors on the surface of tissue mast cells and blood basophils. Mast cells and basophils coated by IgE antibodies are "sensitised." Later exposure to the same allergen cross-links the bound IgE on sensitised cells, resulting in degranulation and the secretion of pharmacologically active mediators such as histamine, leukotriene (LTC4 and LTD4), and prostaglandin that act on the surrounding tissues. The principal effects of these products are vasodilation and smooth-muscle contraction.

Type 1 hypersensitivity can be further classified into an immediate and late-phase reaction. The immediate hypersensitivity reaction occurs minutes after exposure and includes release of vasoactive amines and lipid mediators, whereas the late-phase reaction occurs 2-4 hours after exposure and includes the release of cytokines.

Overview of mediators released by mast cells in type 1 hypersensitivity, and their actions:
Vasodilation and increased permeability
  • Histamine
  • PAF
  • Leukotriene C4, D4 and E4
  • Prostaglandin D2
  • Neutral proteases
Smooth muscle spasm
  • Histamine
  • PAF
  • Leukotriene C4, D4 and E4
  • Prostaglandin
Leukocyte extravasation
  • Cytokines (e.g. chemokines and TNF
  • Leukotriene B4
  • Chemotactic factors for neutrophils and eosinophils
Unless otherwise specified, the reference for this table is:

The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock.

Read more about this topic:  Type I Hypersensitivity

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