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U N I T 4
Infection and Immunity
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).
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.
Complement
activation
Fc receptor
C3b receptor
Phagocyte
Red blood cell
Opsonization, MAC,
phagocytosis
Antibody
A
Complement
activation
Inflammation and
tissue injury
Cell surface
antibody
Leukocytes
Cell membrane
B
Thyroid
epithelial cell
Thyroid hormone
production and release
TSH receptor
Antibody
against TSH
receptor
C
Antibody inhibits binding of
neurotransmitter to receptor
Antibody to
ACh receptor
ACh receptor
Muscle
Acetylcholine
(ACh)
Nerve ending
D
