All of the following are associated with type I hypersensitivity except

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Multiple Choice

All of the following are associated with type I hypersensitivity except

Explanation:
Type I hypersensitivity is driven by IgE antibodies bound to mast cells or basophils. When the allergen re-enters, it cross-links those surface-bound IgE molecules, triggering rapid degranulation and release of preformed mediators like histamine from the mast cells. This immediate release causes the symptoms of the reaction. The presence of a genetic tendency to react to common allergens (atopy) fits with this IgE-mediated pattern, as some individuals are predisposed to produce IgE responses to environmental allergens. Activation of complement is not a defining feature of type I hypersensitivity. The hallmark pathway relies on IgE cross-linking and mast cell degranulation rather than complement-mediated cytotoxicity or inflammation. While complement can be involved in other types of hypersensitivity, the classic immediate type is driven by mast cell mediators, not by complement activation.

Type I hypersensitivity is driven by IgE antibodies bound to mast cells or basophils. When the allergen re-enters, it cross-links those surface-bound IgE molecules, triggering rapid degranulation and release of preformed mediators like histamine from the mast cells. This immediate release causes the symptoms of the reaction. The presence of a genetic tendency to react to common allergens (atopy) fits with this IgE-mediated pattern, as some individuals are predisposed to produce IgE responses to environmental allergens.

Activation of complement is not a defining feature of type I hypersensitivity. The hallmark pathway relies on IgE cross-linking and mast cell degranulation rather than complement-mediated cytotoxicity or inflammation. While complement can be involved in other types of hypersensitivity, the classic immediate type is driven by mast cell mediators, not by complement activation.

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