Defense Mechanisms of the Body
667
body production. If the nonspecifi c defenses are rapidly suc-
cessful, these slowly developing
specifi
c
immune responses may
never play an important role. If the nonspecifi c responses are
only partly successful, the infection may persist long enough for
signifi cant amounts of antibody to be produced. The presence
of antibody leads to both enhanced phagocytosis and direct
destruction of the foreign cells, as well as to neutralization
of any toxins the bacteria secrete. All subsequent encounters
with that type of bacterium will activate the specifi c responses
much sooner and with greater intensity. That is, the person
may have active immunity against that bacteria.
The defenses against viruses in the extracellular fl
uid are
similar, resulting in destruction or neutralization of the virus.
Defenses Against Virus-Infected Cells
and Cancer Cells
The previous section described how antibody-mediated immune
responses constitute the major long-term defense against exog-
enous antigens—bacteria, viruses, and individual foreign mol-
ecules that enter the body and are encountered by the immune
system in the extracellular fl uid. This section now details how
the body’s own cells that have become infected by viruses (or
other intracellular microbes) or transformed into cancer cells
are destroyed.
What is the value of destroying virus-infected host cells?
Such destruction results in release of the viruses into the
extracellular fl uid, where they can be directly neutralized by
circulating antibody, as just described. Generally, only a few
host cells are sacrifi ced in this way, but once viruses have had a
chance to replicate and spread from cell to cell, so many virus-
infected host cells may be killed by the body’s own defenses
that organ malfunction may occur.
Role of Cytotoxic T Cells
Figure 18–18
summarizes a typical cytotoxic T-cell response
triggered by viral infection of body cells. The response triggered
by a cancer cell would be similar. As described earlier, a virus-
infected or cancer cell produces foreign proteins, “endogenous
antigens,” which are processed and presented on the plasma
membrane of the cell complexed with class I MHC proteins.
Cytotoxic T cells specifi c for the particular antigen can bind to
the complex, but just as with B cells, binding to antigen alone
does not cause activation of the cytotoxic T cell. Cytokines
from adjacent activated helper T cells are also needed.
What role do the helper T cells play in these cases? Figure
18–14 illustrates the most likely mechanism. Macrophages
phagocytize free extracellular viruses (or, in the case of can-
cer, antigens released from the surface of the cancerous cells)
Figure 18–18
Summary of events in the killing of virus-
infected cells by cytotoxic T cells. The released
viruses can then be phagocytized. The sequence
would be similar if the inducing cell were a
cancer cell rather than a virus-infected cell.
Carried to all
parts of the body
via blood
Perforin
Perforin
Perforin
Viral
antigen
Macrophage
Class II
MHC
protein
Infected
cell
Virus
Virus
Viral antigen
Infected cells
Channels
Water moves in, cell swells
and dies; virus cannot
replicate and is released
IL-2
and other
cytokines
IL-1
TNF
Cytotoxic
T cell
Helper T cell
To another
infected
cell
Activation
Class I MHC
protein
T-cell receptor
+
+
+
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