Defense Mechanisms of the Body
665
mation had already made capillaries and venules leaky at these
sites) and combine with the type of bacterial surface antigen
that initiated the immune response (see Figure 18–14). These
antibodies then direct the attack (see following discussion)
against the bacteria to which they are now bound.
Thus, immunoglobulins play two distinct roles in
immune responses: (1) during the initial recognition step,
those on the surface of B cells bind to antigen brought to
them; and (2) those secreted by the plasma cells (antibodies)
bind to bacteria bearing the same antigens, “marking” them
as the targets to be attacked.
The Attack: Effects of Antibodies
The antibodies bound to antigen on the microbial surface do not
directly kill the microbe but instead link up the microbe physi-
cally to the actual killing mechanisms—phagocytes (neutrophils
and macrophages), complement, or NK cells. This linkage not
only triggers the attack mechanism but ensures that the killing
effects are restricted to the microbe. Linkage to specifi c antibod-
ies normally protects adjacent normal structures from the toxic
effects of the chemicals employed by the killing mechanisms.
Direct Enhancement of Phagocytosis
Antibodies can act
directly as opsonins. The mechanism is analogous to that for
complement C3b (see Figure 18–5) in that the antibody links
the phagocyte to the antigen. As shown in
Figure 18–15
, the
phagocyte has membrane receptors that bind to the Fc portion
of an antibody. This linkage promotes attachment of the anti-
gen to the phagocyte and the triggering of phagocytosis of the
bacterium.
Activation of the Complement System
As described earlier
in this chapter, the plasma complement system is activated in
nonspecifi
c
infl ammatory responses via the alternate complement
pathway. In contrast, in
specifi
c
immune responses, the presence
of antibody of the IgG or IgM class bound to antigen activates
the
classical complement pathway.
The fi rst molecule in this
pathway, C1, binds to the Fc portion of an antibody that has
combined with antigen (
Figure 18–16
). This results in activa-
tion of the enzymatic portions of C1, thereby initiating the entire
classical pathway. The end product of this cascade, the membrane
attack complex (MAC), can kill the cells the antibody is bound
to by making their membranes leaky. In addition, as we saw in
Bacterium
Extracellular
fluid
Phagocyte
Receptor for Fc
portion of antibody
Antibody
Bacterial antigen
Figure 18–15
Direct enhancement of phagocytosis by
antibody. The antibody links the phagocyte
to the bacterium. Compare this mechanism of
opsonization to that mediated by complement
C3b (see Figure 18–5).
Bacterium
MAC
C3b
binds
Bacterial
antigen
Binding site
for C1
Phagocyte
C3b receptor
C1
Classical
complement
pathway
Extracellular fluid
Figure 18–16
Activation of classical complement pathway by
binding of antibody to bacterial antigen. C1
is activated by its binding to the Fc portion of
the antibody. The membrane attack complex
(MAC) is then generated, along with C3b, which
acts as an opsonin by binding the bacteria to a
phagocyte.
previous page 693 Vander's Human Physiology The Mechanisms of Body Function read online next page 695 Vander's Human Physiology The Mechanisms of Body Function read online Home Toggle text on/off