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Hypersensitivity is defined as an abnormal, exaggerated immune reaction to a foreign agent, with resulting injury to host tissues. Four different mechanisms of hypersensitivity have been elucidated (Table 8-1). All forms except type IV are mediated by humoral mechanisms (ie, by antibodies); type IV hypersensitivity is cell-mediated. In all forms, initial exposure (sensitizing dose) to the antigen involved evokes a primary immune response (sensitization). Following a short period (1 or more weeks) during which the immune system is activated, a hypersensitivity response occurs upon any subsequent exposure (challenge dose) to that antigen.

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Table Graphic Jump Location
Table 8–1. Hypersensitivity Mechanisms.
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Type I (Immediate) Hypersensitivity (Atopy; Anaphylaxis)

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Mechanism

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(Figure 8-1.) The first exposure to an antigen (allergen) activates the immune system and causes production of IgE antibodies (reagins) specifically reactive against the antigen. These become attached to the surface membrane of mast cells and basophils through high-affinity IgE Fc receptors. Production of sufficient antibody to develop clinical hypersensitivity takes 1 or more weeks. When subsequent exposure to the same antigen occurs, an antigen-antibody (IgE) interaction takes place on the surface of the mast cell or basophil and causes degranulation of these cells. The cytoplasmic granules of mast cells release vasoactive substances (histamine and a variety of enzymes that generate bradykinin and leukotrienes [Chapter 3: The Acute Inflammatory Response]) that cause vasodilation, increased vascular permeability, and smooth muscle contraction. Mast cells also release factors that are chemotactic for neutrophils and eosinophils; many lesions caused by type I hypersensitivity contain numerous eosinophils in affected tissues and peripheral blood. Eosinophils activate both the coagulation and complement systems and promote further degranulation of basophils and mast cells. However, eosinophils also release arylsulfatase B and histaminase, which serve to cleave leukotrienes and histamine, respectively, thereby down-modulating the allergic response.

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Figure 8–1.
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Type I hypersensitivity. The first (sensitizing) dose of antigen results in production of specifically reactive IgE that becomes adsorbed on the surface of mast cells. A second exposure to the antigen results in an antigen-antibody reaction on the mast cell surface, causing rapid release by the mast cell of vasoactive substances responsible ...

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