346
U N I T 4
Infection and Immunity
(see Chapter 3). The leukotrienes and prostaglandins
produce responses similar to histamine, although their
effects are delayed and prolonged by comparison. Mast
cells also produce cytokines and chemotactic factors
that prompt the influx of eosinophils and leukocytes to
the site of allergen contact, additionally contributing to
the inflammatory response.
At this point, it is important to note that not all
IgE-mediated responses produce discomfort and dis-
ease. Type I hypersensitivity, particularly the late-
phase response, plays a protective role in the control
of parasitic intestinal infections. IgE antibodies
directly damage the larvae of these parasites by recruit-
ing inflammatory cells and causing antibody-depen-
dent cell-mediated cytotoxicity. This type of type I
hypersensitivity reaction is particularly important in
developing countries where much of the population is
infected with intestinal parasites.
Systemic (Anaphylactic) Reactions
Anaphylaxis is a systemic life-threatening hypersen-
sitivity reaction characterized by widespread edema,
difficulty breathing, and vascular shock secondary to
vasodilation
2,6–8
(see section on anaphylactic shock,
Chapter 20). It results from the presence of antigen
introduced by injection, insect sting, or absorption
across the epithelial surface of the skin or gastroin-
testinal mucosa. The level of severity depends on the
level of sensitization. Even small amounts of antigen,
Release of cytokines
Degranulation and
release of mediators
Membrane phospholipids
Secondary late response
Primary early response
Antigen
CD4
IL-4
IL-3, IL-5
Eosinophil
recruitment
Antibody
Mast cell
Sensitization
of mast cell
or basophil
Recruitment and activation
of inflammatory cells
Arachidonic acid
Prostaglandins Leukotrienes
Vasodilation
Vascular damage
Smooth muscle spasm
Mucosal edema
Mucus secretion
Leukocyte infiltration
Epithelial damage
Bronchospasm
B cell
IgE-secreting
plasma cell
T
H
2
Basophil
FIGURE 16-1.
Type I, IgE-mediated
hypersensitivity reaction.The
stimulation of B-cell differentiation
by an antigen-stimulated type 2
helperT (T
H
2) cell leads to plasma
cell production of IgE and mast
cell or basophil sensitization.
Subsequent binding of the antigen
produces degranulation of the
sensitized mast cell or basophil
with release of preformed
mediators that leads to a primary,
or early-phase, response.T
H
2T-cell
recruitment of eosinophils, along
with the release of cytokines and
membrane phospholipids from the
mast cell, leads to a secondary,
or late-phase, response. IgE,
immunoglobulin E; IL, interleukin.
