Porth's Essentials of Pathophysiology, 4e

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Infection and Immunity

U N I T 4

or it may occur after ingestion of any food. Exercise without ingestion of the incriminated food does not produce symptoms. Food allergies can occur at any age but, similar to atopic dermatitis and rhinitis, they tend to manifest dur- ing childhood. The allergic response is thought to occur when there is contact between specific food allergens and sensitizing IgE in the intestinal mucosa, thereby causing local and systemic release of histamine and other media- tors of the allergic response. In this disorder, allergens usually are food proteins and partially digested food products. Carbohydrates, lipids, or food additives, such as preservatives, colorings, or flavorings, also are poten- tial allergens. Closely related food groups can contain common cross-reacting allergens. For example, some persons are allergic to all legumes (i.e., beans, peas, and peanuts). Diagnosis of food allergies usually is based on a care- ful food history and through provocative diet testing. Provocative testing involves careful elimination of a sus- pected allergen from the diet for a period of time to see if the symptoms disappear and reintroducing the food to see if the symptoms reappear. Only one food should be tested at a time. Treatment focuses on avoidance of

the food or foods responsible for the allergy. However, avoidance may be difficult for persons who are exqui- sitely sensitive to a particular food protein because foods may be contaminated with the protein dur- ing processing or handling of the food. As mentioned previously, contamination may occur when chocolate candies without peanuts are processed with the same equipment used for making candies with peanuts. Type II, Antibody-Mediated Disorders Type II (antibody-mediated) hypersensitivity reactions are mediated by IgG or IgM antibodies directed against target antigens on cell surfaces or in connective tis- sues. 2,3 The antigens may be endogenous antigens that are present on the membranes of body cells, or they may be exogenous antigens, such as drug metabolites, that are adsorbed on the membrane surface. Three different antibody-mediated mechanisms are involved in type II reactions: (1) complement- and antibody–mediated cell destruction, (2) complement- and antibody-mediated inflammation, and (3) antibody-mediated cellular dysfunction 2 (Fig. 16-2).

Cell membrane

Cell surface antibody

Red blood cell

Antibody

Fc receptor

C3b receptor

Phagocyte

Complement activation

Complement activation

Leukocytes

FIGURE 16-2. Type II, hypersensitivity reactions result from binding of antibodies to normal or altered surface antigens. (A) Opsonization and complement- or antibody receptor– mediated phagocytosis or cell lysis through membrane attack complex (MAC). (B) Complement- and antibody receptor–mediated inflammation resulting from recruitment and activation of inflammation-producing leukocytes (neutrophils and monocytes). Antibody-mediated cellular dysfunction, in which (C) antibody against the thyroid-stimulating hormone (TSH) receptor increases thyroid hormone production. (D) Antibody to acetylcholine receptor inhibits receptor binding of the neurotransmitter in myasthenia gravis.

Opsonization, MAC, phagocytosis

Inflammation and tissue injury

B

A

Antibody against TSH receptor

Nerve ending

TSH receptor

Acetylcholine (ACh)

Thyroid epithelial cell

Antibody to ACh receptor ACh receptor Muscle

Thyroid hormone production and release

Antibody inhibits binding of neurotransmitter to receptor

C

D