synonymous; both terms refer to the altered state induced by an antigen, in which pathological reactions can be subsequently elicited by that antigen or by a structurally similar substance. Within the context of the allergic response the antigen is usually referred to as the "allergen," and the immunized individual, previously called immune, is called sensitive, hypersensitive, or allergic.

Allergic responses were originally divided into two classes, immediate and delayed, on the basis of the lag in their appearance—several minutes after the administration of antigen in the former, and several hours or even a few days in the latter. These terms are still used, but they are now endowed with a different meaning. Not only the reactions that appear within minutes, but also some of the more slowly evolving ones, are mediated by freely diffusible antibody molecules. To emphasize this common feature, both are now called immediate type responses (although "immediate" is not to be taken literally). In contrast, the delayed type are those slowly evolving responses that are mediated by specifically reactive ("sensitized") T lymphocytes rather than by freely diffusible antibody molecules; hence they are also called cell-mediated hypersensitivity. They constitute part of a larger group of reactions, called cell-mediated immunity, in which similar mechanisms are also involved in resistance to many infectious agents and to neoplastic cells.

Chapters 1 and 2 of this report provide general descriptions of concepts and definitions related to sensitization, hypersensitivity, and IgE-mediated allergy. To recapitulate in summary, allergic disease occurs when a susceptible individual is exposed to an allergen and becomes sensitized. Additional exposure to the sensitizing allergen leads to the development of an allergic reaction through the release of histamine and other chemicals from mast cells. Exposure to other substances (e.g., environmental tobacco smoke) may serve to promote the development of allergic reactions and disease.

The typical allergic reaction such as hay fever begins when allergenic proteins from substances such as grass pollen, are inhaled by a sensitive individual and pass through the nasal mucosa. The inhaled allergens then interact with IgE antibodies on the surface of mast cells in the mucosa to cause the release of histamine and other bioactive mediators. These mediators, in turn, cause vasodilation of blood vessels and stimulate secretory cells. The result is the clinical symptomatology and manifestations of nasal congestion, rhinorrhea, and conjunctivitis commonly associated with allergies.

As discussed previously in this report, nearly 20 percent of the population suffer to a greater or lesser degree with allergies involving localized anaphylactic reactions to extrinsic allergens such as grass pollen, animal dander, mites in house dust, and so on. Contact of the allergen with cell-bound IgE in the bronchial tree results in asthma, in the nasal mucosa results in hay fever, and in the conjunctival tissues results in allergic conjunctivitis.



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