It is commonly taught that type I hypersensitivity reactions are caused by the interaction of mast cell-bound IgE with allergen molecules. The resulting mast cell degranulation releases inflammatory mediators, including histamine and arachidonic acid metabolites.
Evidence for the role of IgE includes experiments in the mouse (the passive cutaneous anaphylaxis model) where IgE-containing serum may transfer allergen-specific hypersensitivity.
In contrast, recent research has demonstrated that genetically engineered mice, deficient in IgE, are susceptible to anaphylaxis. Other models of passive cutaneous anaphylaxis propose an alternative IgG-mediated pathway for type I hypersensitivity reactions.
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