NBME Immunology Practice Test

This question targets IgE-mediated immediate hypersensitivity. In this type, exposure to an allergen first leads to IgE production by B cells under the influence of Th2 cytokines (like IL-4). The produced IgE binds to FcεRI receptors on mast cells and basophils, sensitizing them. Upon subsequent exposure, the allergen cross-links the bound IgE, triggering rapid degranulation of these cells and release of mediators such as histamine, leukotrienes, and prostaglandins. These mediators cause immediate effects: vasodilation and increased vascular permeability (edema), smooth muscle contraction (bronchoconstriction), and mucous secretion, producing symptoms like hives, runny nose, wheezing, or, in severe cases, anaphylaxis. The hallmark is that this reaction is IgE-dependent and occurs within minutes of exposure. In contrast, other hypersensitivities involve different mechanisms: antibody-mediated cytotoxic reactions use IgG or IgM against cell surfaces or tissues; immune complex–mediated reactions involve deposition of antigen–antibody complexes; and T cell–mediated delayed-type hypersensitivity relies on sensitized T cells rather than antibodies and takes longer to manifest.