Type I Hypersensitivity Reaction (Cytotropic / Anaphylactic Reaction )
Type I hypersensitivity is an immediate, antibody-mediated reaction characterized by rapid onset after exposure to an allergen.
Also called anaphylactic or IgE-mediated hypersensitivity.
Mediated by IgE antibodies bound to mast cells and basophils.
Key Features
Rapid reaction (seconds to minutes).
Involves pre- formed antibodies and mediators.
Can be local (e.g., allergic rhinitis) or systemic (e.g., anaphylactic shock).
Phases of Reaction
1 Sensitization phase
First exposure to allergen → antigen processed by antigen-presenting cells (APCs).
Activation of Th2 cells → cytokines (IL- 4, IL- 5, IL- 13).
B cells class switch to IgE production.
IgE binds to high-affinity FcεRI receptors on mast cells and basophils.
Individual is now "sensitized".
2 Activation phase (re- exposure)
Allergen cross-links bound IgE on mast cells → rapid degranulation.
Release of pre- formed and newly synthesized mediators.
Mediators of Type I Hypersensitivity
Pre- formed mediators (immediate release)
Histamine: vasodilation, increased vascular permeability, bronchoconstriction, mucus secretion.
Heparin: anticoagulant.
Enzymes: tryptase, chymase → tissue remodeling.
Newly synthesized mediators
Lipid-derived mediators:
- Leukotrienes (C4, D4, E4): potent bronchoconstrictors, increase
vascular permeability.
- Prostaglandin D2: bronchospasm, vasodilation.
- Platelet- activating factor (PAF): chemotaxis, activation of other cells.
Cytokines:
- TNF- α: promotes inflammation.
- IL-4, IL-5: promote eosinophil activation and further IgE production.