Chapter 18
Figure 18–5, another activated complement molecule (C3b)
functions as an opsonin to enhance phagocytosis of the microbe
by neutrophils and macrophages (see Figure 18–16). Thus, anti-
bodies enhance phagocytosis both directly (see Figure 18–15)
and via activation of complement C3b.
It is important to note that C1 binds not to the unique
antigen binding sites in the antibody’s prongs, but rather to
complement binding sites in the Fc portion. Because the lat-
ter are the same in virtually all antibodies of the IgG and IgM
classes, the complement molecule will bind to
bound antibodies belonging to these classes. In other words,
there is only one set of complement molecules, and once acti-
vated, they do essentially the same thing regardless of the spe-
cifi c identity of the invader.
Antibody-Dependent Cellular Cytotoxicity
We have seen
that both a particular complement molecule (C1) and a phago-
cyte can bind nonspecifi cally to the Fc portion of an antibody
bound to antigen. NK cells can also do this (just substitute an
NK cell for the phagocyte in Figure 18–15). Thus, antibodies
can link target cells to NK cells, which then kill the targets
directly by secreting toxic chemicals. This is called
dependent cellular cytotoxicity (ADCC)
because the kill-
ing (cytotoxicity) is carried out by cells (NK cells), but the
process depends upon the presence of antibody. Note that it is
the antibodies that confer specifi
city upon ADCC, just as they
do on antibody-dependent phagocytosis and complement acti-
vation. This mechanism for bringing NK cells into play is the
one exception, mentioned earlier, to the generalization that the
mechanism by which NK cells identify their targets is unclear.
Direct Neutralization of Bacterial Toxins and Viruses
Toxins secreted by bacteria into the extracellular fl uid can act as
antigens to induce antibody production. The antibodies then
combine with the free toxins, thus preventing interaction of
the toxin with susceptible cells. Because each antibody has two
binding sites for antigen, clump-like chains of antibody-antigen
complexes form, and these clumps are then phagocytized.
A similar binding process occurs as part of the major
antibody-mediated mechanism for eliminating viruses in the
extracellular fl uid. Certain of the viral surface proteins serve
as antigens, and the antibodies produced against them com-
bine with them, preventing attachment of the virus to plasma
membranes of potential host cells. This prevents the virus
from entering a cell. As with bacterial toxins, chains of anti-
body-virus complexes are formed and can be phagocytized.
Active and Passive Humoral Immunity
The response of the antibody-producing machinery to inva-
sion by a foreign antigen varies enormously, depending upon
whether the machinery has previously been exposed to that
antigen. Antibody production occurs slowly over several weeks
following the fi rst contact with an antigen, but any subsequent
infection by the same invader elicits an immediate and con-
siderable outpouring of additional specifi c antibodies (
). This response, which is mediated by the memory B
cells described earlier, confers a greatly enhanced resistance
toward subsequent infection with that particular microorgan-
ism. Resistance built up as a result of the body’s contact with
microorganisms and their toxins or other antigenic compo-
nents is known as
active immunity.
Until the twentieth century, the only way to develop
active immunity was to suffer an infection, but now the injec-
tion of microbial derivatives in vaccines is used. A
consist of small quantities of living or dead microbes, small
quantities of toxins, or harmless antigenic molecules derived
from the microorganism or its toxin. The general principle is
always the same: Exposure of the body to the agent results in
an active immune response along with the induction of the
memory cells required for rapid, effective response to possible
future infection by that particular organism.
A second kind of immunity, known as
passive immunity,
is simply the direct transfer of antibodies from one person to
another, the recipient thereby receiving preformed antibodies.
Such transfers occur between mother and fetus because IgG can
move across the placenta. Also, breast-fed children receive IgA
antibodies in the mother’s milk. These are important sources of
protection for the infant during the fi rst months of life, when
the antibody-synthesizing capacity is relatively poor.
The same principle is used clinically when specifi c anti-
bodies (produced by genetic engineering) or pooled gamma
globulin is given to patients exposed to or suffering from cer-
tain infections such as hepatitis. Because antibodies are pro-
teins with a limited life span, the protection afforded by this
transfer of antibodies is relatively short-lived, usually lasting
only a few weeks or months.
It is now possible to summarize the interplay between non-
specifi c and specifi c immune defenses in resisting a bacterial
infection. When a particular bacterium is encountered for
the fi rst time,
defense mechanisms resist its entry
and, if entry is gained, attempt to eliminate it by phagocy-
tosis and nonphagocytic killing in the infl
ammatory process.
Simultaneously, bacterial antigens induce the relevant specifi c
B-cell clones to differentiate into plasma cells capable of anti-
Figure 18–17
Rate of antibody production following initial exposure to an antigen
and subsequent exposure to the same antigen.
1st antigen
2nd antigen
Time (months)
Amount of specific antibody in plasma
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