654
Chapter 18
Figure 18–6
Role of interferon in preventing viral replication. (a) Most cell types, when infected with viruses, secrete interferon, which enters the interstitial
fl uid and binds to interferon receptors on the secreting cells themselves (autocrine function), and (b) adjacent cells (paracrine function).
In addition, some interferon enters the blood and binds to interferon receptors on far-removed cells (endocrine function). The binding of
interferon to its receptors induces the synthesis of proteins (c) that inhibit viral replication should viruses enter the cell (d).
Figure 18–6
physiological
inquiry
Are there other examples besides immune secretions in which a single substance may act as both an endocrine and paracrine agent?
Answer can be found at end of chapter.
Bacterium
Phagocyte
Extracellular fluid
C3b receptor
C3b
Nucleus
Figure 18–5
Function of complement C3b as an opsonin. One portion of
C3b binds nonspecifi cally to carbohydrates on the surface of the
bacterium, whereas another portion binds to specifi c receptor sites
for C3b on the plasma membrane of the phagocyte. The structures
are not drawn to scale.
No
replication
Antiviral
protein
Interferon
Interferon
receptor
Virus
(a)
(b)
(c)
(d)
Other Opsonins in Nonspecifi c Defenses
In addition to complement C3b, other plasma proteins can
bind nonspecifi
cally to carbohydrates or lipids in the cell wall
of microbes and facilitate opsonization. Many of these, for
example
C-reactive protein,
are produced by the liver and
are always found at some concentration in the plasma. Their
production and plasma concentrations, however, are greatly
increased during infl
ammation.
Tissue Repair
The fi nal stage of infl
ammation is tissue repair. Depending
upon the tissue involved, multiplication of organ-specifi c cells
by cell division may or may not occur during this stage. For
example, liver cells multiply but skeletal muscle cells do not. In
any case, fi broblasts (a type of connective tissue cell) that reside
in the area divide rapidly and begin to secrete large quantities
of collagen, while blood vessel cells proliferate in the process of
angiogenesis. All of these events are brought about by chemi-
cal mediators, particularly a group of locally produced growth
factors. Finally, remodeling occurs as the healing process winds
down. The fi nal repair may be imperfect, leaving a scar.
Interferons
Interferons
are a family of cytokines that nonspecifi cally inhibit
viral replication inside host cells. In response to infection by
a virus, most cell types produce interferons and secrete them
into the extracellular fl uid. Interferons then bind to plasma
membrane receptors on the secreting cell and on other cells,
whether they are infected or not (
Figure 18–6
). This binding
triggers the synthesis of dozens of different antiviral proteins
by the cell. If the cell is already infected or eventually becomes
infected, these proteins interfere with the ability of the viruses
to replicate.
Interferons are not specifi c. Many kinds of viruses induce
interferon synthesis, and interferons in turn can inhibit the
multiplication of many kinds of viruses.
Specifi c Immune Defenses
Because of the complexity of specifi c immune defenses, it is
useful to present a brief orientation before describing in more
detail the various components of the response.
Overview
Lymphocytes are the essential cells in specifi c immune defenses.
Unlike nonspecifi c defense mechanisms, lymphocytes must
recognize the specifi c foreign matter to be attacked. Any for-
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