response, in large part by activating the complement system.
Complement proteins mediate many steps of inﬂ
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
Harmful Immune Responses
I. Rejection of tissue transplants is initiated by MHC proteins on
the transplanted cells and is mediated mainly by cytotoxic T
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
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
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
acute phase protein
acute phase response
antigen binding site
B lymphocyte (B cell)
Class I MHC protein
Class II MHC protein
cytotoxic T cell
helper T cell
interleukin 1 (IL-1)
interleukin 2 (IL-2)
interleukin 6 (IL-6)
membrane attack complex
MHC protein (class I and
natural killer (NK) cell
nonspeciﬁ c immune
primary lymphoid organ
secondary lymphoid organ
speciﬁ c immune defense
T lymphocyte (T cell)
tumor necrosis factor