796
UNIT 4
Maintenance of the Body
21
Stem cells of the immune system originate in the liver and spleen
during weeks 1–9 of embryonic development. Later the bone
marrow becomes the predominant source of stem cells, and
it persists in this role into adult life. As we have seen, the lym-
phocyte precursors develop self-tolerance and immunocompe-
tence in their “programming organs” (thymus and bone marrow)
and then populate other lymphoid tissues.
Te newborn’s immune system depends primarily on an-
tibodies, and hence on ±
H
2 lymphocytes. Te ±
H
1 system is
educated and gets stronger as a result of encounters with
microbes—both harmful and harmless. If such exposure and
education does not occur, immune balance is upset and the ±
H
2
system flourishes, causing the immune system to teeter toward
allergies. Unhappily, the desire to keep our children squeaky
clean with antibiotics that kill off both harmful and harmless
bacteria may derail normal immune development.
A wide variety of factors outside the immune system influ-
ence immune function. For example:
Nervous system.
Te study of psychoneuroimmunology—a
brain-twisting term coined to describe links between the brain
and the immune system—helps explain how depression, emo-
tional stress, and grief can impair the immune response.
Diet.
Recently, researchers have discovered that vitamin D is
required for activation of CD8 cells to become ±
C
cells. Tis
may explain the finding of a clinical trial in which vitamin D
supplements reduced the incidence of seasonal influenza in
children. On the other hand, vitamin D deficiency has been
linked with autoimmune diseases such as multiple sclerosis.
Te immune system normally serves us very well until late in
life. Ten its efficiency begins to wane, and its ability to fight in-
fection declines. Old age is also accompanied by greater suscep-
tibility to both immunodeficiency and autoimmune diseases.
Te greater incidence of cancer in the elderly may also reflect
the progressive failure of the immune system. We do not know
why the immune system begins to fail, but we do know that the
thymus begins to atrophy a²er puberty and the production of
naive ± and B cells declines with age, possibly because progeni-
tor cells reach the limits of their ability to divide.
■ ■ ■
Our amazingly diverse adaptive defenses are regulated by cel-
lular interactions and a flood of chemicals. ± cells and antibodies
make perfect partners. Antibodies respond swi²ly to toxins and
molecules on the outer surfaces of foreign organisms, and ± cells
destroy foreign antigens hidden inside cells and our own cells that
have become mutinous (cancer cells). Te innate immune sys-
tem exhibits a different arsenal for body defense, an arsenal that
is simpler perhaps and more easily understood. Te innate and
adaptive defenses are tightly interlocked, each providing what the
other cannot and amplifying each other’s effects.
their onset is slower (1–3 hours a²er antigen exposure) and the
reaction lasts longer (10–15 hours).
Cytotoxic (type II) reactions
occur when antibodies bind to
antigens on specific body cells and stimulate phagocytosis and
complement-mediated lysis of the cellular antigens. Cytotoxic
hypersensitivity may occur a²er a patient has received a trans-
fusion of mismatched blood and complement lyses the foreign
red blood cells.
Immune-complex (type III) hypersensitivities
result when
antigens are widely distributed through the body or blood and the
huge number of insoluble antigen-antibody complexes formed
cannot be cleared from a particular area. (Tis may reflect a per-
sistent infection or an autoimmune disease.) An intense inflam-
matory reaction occurs, complete with complement-mediated
cell lysis and cell killing by neutrophils that severely damages lo-
cal tissues. Examples of type III hypersensitivity are
farmer’s lung
(induced by inhaling moldy hay) and the glomerulonephritis of
systemic lupus erythematosus.
Delayed Hypersensitivities
Delayed (type IV) hypersensitivity reactions
are caused by
± cells and take longer to appear (1–3 days) than antibody-
mediated hypersensitivity reactions. Inflammation and tissue
damage result from the action of cytokine-activated macro-
phages, and sometimes cytotoxic ± cells.
Te most familiar examples of delayed hypersensitivity reac-
tions are those classified as
allergic contact dermatitis
which
follow skin contact with poison ivy, some metals (nickel in
jewelry), and certain cosmetic and deodorant chemicals. Tese
agents act as haptens (see p. 774), and a²er they diffuse through
the skin and attach to self-proteins, the immune system per-
ceives them as foreign.
Skin tests for tuberculosis depend on a delayed hypersensi-
tivity reaction. When the tubercle antigens are introduced just
under the skin, a small hard lesion forms that persists for days if
the person has been sensitized to the antigen.
Check Your Understanding
22.
What makes HIV particularly hard for the immune system to
defeat?
23.
What event triggers the release of histamine from mast cells
in an allergic response?
For answers, see Appendix H.
Developmental Aspects
of the Immune System
Describe changes in immunity that occur with aging.
Briefly describe the role of the nervous system in regulating
the immune response.
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