680
Chapter 18
response, in large part by activating the complement system.
Complement proteins mediate many steps of infl
ammation,
act as opsonins, and directly kill antibody-bound cells via
the membrane attack complex.
e. Antibodies of the IgG class also act directly as opsonins and
link target cells to NK cells, which directly kill the target cells.
f. Antibodies also neutralize toxins and extracellular viruses.
XII. Virus-infected cells and cancer cells are killed by cytotoxic
T cells, NK cells, and activated macrophages.
a. A cytotoxic T cell binds, via its membrane receptor, to
cells bearing a viral antigen or cancer-associated antigen in
association with a class I MHC protein.
b. Activation of the cytotoxic T cell also requires cytokines
secreted by helper T cells, themselves activated by antigen
presented by a macrophage. The cytotoxic T cell then
releases perforin, which kills the attached target cell by
making it leaky.
c. NK cells and macrophages are also stimulated by helper
T-cell cytokines, particularly IL-2 and interferon-gamma, to
attack and kill virus-infected or cancer cells.
Systemic Manifestations of Infection
I. The acute phase response is summarized in Figure 18–20.
II. The major mediators of this response are IL-1, TNF, and IL-6.
Factors that Alter the Body’s Resistance to Infection
I. The body’s capacity to resist infection is infl uenced by
nutritional status, the presence of other diseases, psychological
factors, and the intactness of the immune system.
II. AIDS is caused by a retrovirus that destroys helper T cells and
therefore reduces the ability to resist infection and cancer.
III. Antibiotics interfere with the synthesis of macromolecules by
bacteria.
Harmful Immune Responses
I. Rejection of tissue transplants is initiated by MHC proteins on
the transplanted cells and is mediated mainly by cytotoxic T
cells.
II. Transfusion reactions are mediated by antibodies.
a. Transfused erythrocytes will be destroyed if the recipient
has natural antibodies against the antigens (type A or type
B) on the cells.
b. Antibodies against Rh-positive erythrocytes can be
produced following the exposure of an Rh-negative person
to such cells.
III. Allergies (hypersensitivity reactions) caused by allergens are of
several types.
a. In delayed hypersensitivity, the infl
ammation is due to
the interplay of helper T cell cytokines and macrophages.
Immune-complex hypersensitivity is due to complement
activation by antigen-antibody complexes.
b. In immediate hypersensitivity, antigen binds to IgE
antibodies, which are themselves bound to mast cells. The
mast cells then release infl ammatory mediators such as
histamine that produce the symptoms of allergy. The late
phase of immediate hypersensitivity is mediated by eosinophils.
IV. Autoimmune attacks are directed against the body’s own
proteins, acting as antigens. Reasons for the failure of immune
tolerance are summarized in Table 18–11.
V. Normal tissues can be damaged by excessive infl
ammatory
responses to microbes.
Additional Clinical Examples
I. Systemic lupus erythematosus (SLE) is an autoimmune
disease in which several antigens on different types of cells are
mistakenly recognized as “nonself.”
II. The major clinical problems in SLE are nephritis, anemia, and
thrombocytopenia.
KEY TERMS
activated macrophage
668
active immunity
666
acute phase protein
670
acute phase response
668
adenoid
656
adhesion molecule
651
alternate complement
pathway
653
antibody
658
antibody-dependent cellular
cytotoxicity (ADCC)
666
antibody-mediated
response
658
antigen
655
antigen binding site
658
antigen presentation
660
antigen-presenting cell
(APC)
660
B lymphocyte (B cell)
657
chemoattractant
651
chemokine
651
chemotaxin
651
chemotaxis
651
classical complement
pathway
665
Class I MHC protein
660
Class II MHC protein
660
clonal deletion
662
clonal expansion
655
clonal inactivation
662
clone
655
complement
652
costimulus
661
C3b
653
C-reactive protein
654
cytokine
648
cytotoxic T cell
658
dendritic cell
647
diapedesis
651
epitope
661
Fc
658
gamma globulin
664
helper T cell
658
histamine
674
hydrogen peroxide
652
IgA
664
IgD
664
IgE
664
IgG
664
IgM
664
immune surveillance
646
immune system
647
immune tolerance
662
immunoglobulin
658
immunology
646
infl
ammation
648
interferon
654
interferon-gamma
668
interleukin 1 (IL-1)
661
interleukin 2 (IL-2)
663
interleukin 6 (IL-6)
670
leukocyte
647
lymph node
656
lymphocyte
648
lymphocyte activation
655
lymphoid organ
655
macrophage
647
macrophage-like cell
647
major histocompatibility
complex (MHC)
660
margination
651
mast cell
648
membrane attack complex
(MAC)
653
memory cell
655
MHC protein (class I and
class II)
660
natural killer (NK) cell
658
nitric oxide
652
nonspecifi c immune
defense
646
opsonin
652
passive immunity
666
perforin
668
phagocyte
648
phagocytosis
648
phagolysosome
652
phagosome
652
plasma cell
647
primary lymphoid organ
655
Rh factor
673
secondary lymphoid organ
655
specifi c immune defense
646
spleen
656
T lymphocyte (T cell)
658
thymopoietin
656
thymus
656
tonsil
656
tumor necrosis factor
(TNF)
661
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