Type I hypersensitivity is an immediate, IgE-mediated reaction, occurring within minutes of re-exposure to an antigen (allergen) in a previously sensitized individual — the classical “allergic” reaction.
Mechanism:
Sensitization phase: on first exposure to an allergen, susceptible (atopic) individuals mount a Th2-skewed response, producing allergen-specific IgE, which binds via its Fc portion to high-affinity FcεRI receptors on the surface of mast cells and basophils — the individual is now “sensitized” but asymptomatic.
Effector phase: on re-exposure, the allergen cross-links adjacent IgE molecules on the sensitized mast cell/basophil surface, triggering degranulation — immediate release of pre-formed mediators (histamine, tryptase) and rapid synthesis of new mediators (leukotrienes, prostaglandins, platelet-activating factor).
These mediators cause vasodilation, increased vascular permeability, smooth muscle contraction (bronchospasm), and increased mucus secretion — producing the immediate clinical response within minutes.
A late-phase reaction (4–8 hours later) follows, driven by recruited eosinophils, neutrophils, and Th2 cells, sustaining inflammation.
Laboratory diagnosis: skin prick testing, serum total and allergen-specific IgE (RAST/ImmunoCAP), peripheral eosinophil count.
Management: allergen avoidance, antihistamines (H1 blockers) for mild reactions, adrenaline (epinephrine) as first-line emergency treatment for anaphylaxis, and allergen-specific immunotherapy for long-term desensitization in selected cases.
