Describe the IgE-mediated type I hypersensitivity mechanism and the mediators released during the effector phase.

• A. Allergen exposure leads to IgE production and sensitization of mast cells; upon re-exposure, cross-linking of IgE triggers mast cell degranulation releasing histamine, leukotrienes, prostaglandins, and cytokines causing immediate symptoms.
• B. IgG-mediated immune complex deposition.
• C. T-cell mediated delayed hypersensitivity.
• D. Complement-mediated lysis.

Answer: (A)

In this mechanism, the body first becomes sensitized when an allergen triggers production of allergen-specific IgE that binds to high-affinity FcεRI receptors on mast cells and basophils. Upon re-exposure, the allergen cross-links the bound IgE, causing rapid degranulation of these cells. This release brings out preformed mediators and newly made ones that drive the symptoms of an immediate hypersensitivity reaction.

The immediate effector mediators include histamine, which causes vasodilation and increased vascular permeability (leading to redness, swelling, and mucus production) and bronchoconstriction. In addition, newly synthesized leukotrienes and prostaglandins amplify bronchial smooth muscle contraction and vascular changes, while cytokines released during the reaction (such as IL-4, IL-5, and IL-13) sustain and shape the inflammatory response, recruit eosinophils, and promote ongoing IgE production. The result is the quick onset of symptoms like itching, swelling, runny nose, hives, or even anaphylaxis in severe cases. There is also a late-phase response driven by recruited inflammatory cells that can prolong symptoms.

Other options describe different hypersensitivity pathways: IgG immune complexes cause type III reactions; T cells mediate delayed-type hypersensitivity (type IV); and complement-mediated lysis is not the defining feature of this IgE-driven mechanism.