Chapter 21
The Immune System: Innate and Adaptive Body Defenses
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21
neutrophils encounter these CAMs, they slow and roll along
the surface, eventually achieving an initial foothold. When
activated by inflammatory chemicals, CAMs on neutrophils
bind tightly to endothelial cells.
Margination
refers to this
phenomenon of phagocytes clinging to the inner walls (mar-
gins) of the capillaries and postcapillary venules.
3
Diapedesis.
Continued chemical signaling prompts the
neutrophils to flatten and squeeze between the endothelial
cells of the capillary walls—a process called
diapedesis
.
4
Chemotaxis.
Inflammatory chemicals act as homing devices,
or more precisely
chemotactic agents
. Neutrophils and other
WBCs migrate up the gradient of chemotactic agents to the
site of injury (positive
chemotaxis
). Within an hour aFer the
inflammatory response has begun, neutrophils have collected
at the site and are devouring any foreign material present.
As the body’s counterattack continues, monocytes follow neu-
trophils into the injured area. Monocytes are fairly poor phago-
cytes, but within 12 hours of leaving the blood and entering the
tissues, they swell and develop large numbers of lysosomes, be-
coming macrophages with insatiable appetites. Tese late-arriving
macrophages replace the neutrophils on the battlefield.
Macrophages are the central actors in the final disposal of
cell debris as an acute inflammation subsides, and they pre-
dominate at sites of prolonged, or
chronic
, inflammation. Te
ultimate goal of an inflammatory response is to clear the in-
jured area of pathogens, dead tissue cells, and any other debris
delivers important proteins such as complement and clotting
factors to the interstitial fluid (±igure 21.3).
Te clotting factors form a gel-like fibrin mesh (a clot) that
acts as a scaffold for permanent repair. Te mesh also isolates
the injured area and prevents bacteria and other harmful agents
from spreading. Walling off the injured area is such an impor-
tant defense strategy that some bacteria (such as
Streptococcus
)
have evolved enzymes that break down the clot, allowing them
to invade surrounding tissues.
Phagocyte Mobilization
Soon aFer inflammation begins, phagocytes flood the dam-
aged area. Neutrophils lead, followed by macrophages. If path-
ogens provoked the inflammation, a group of plasma proteins
known as complement is activated and elements of adaptive
immunity (lymphocytes and antibodies) also arrive at the
injured site.
Figure 21.4
illustrates the four steps in which
phagocytes are mobilized to infiltrate the injured site.
1
Leukocytosis.
Injured cells release chemicals called
leuko-
cytosis-inducing factors
. In response, neutrophils enter
blood from red bone marrow and within a few hours, the
number of neutrophils in blood increases four- to five-
fold. Tis
leukocytosis,
the increase in white blood cells
(WBCs), is characteristic of inflammation.
2
Margination.
Inflamed endothelial cells sprout cell adhe-
sion molecules (CAMs) that signal “this is the place.” As
1
2
3
4
Leukocytosis.
Neutrophils enter
blood from bone
marrow.
Margination.
Neutrophils cling
to capillary wall.
Diapedesis.
Neutrophils flatten
and squeeze out of
capillaries.
Chemotaxis.
Neutrophils
follow chemical
trail.
Inflammatory
chemicals
diffusing from
the inflamed
site act as
chemotactic
agents.
Capillary wall
Basement
membrane
Endothelium
Innate defenses
Internal defenses
Figure 21.4
Phagocyte mobilization.
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