Human Physiology, 14th edition (2016)

(Tina Sui) #1

514 Chapter 15


Some tumor cells, unfortunately, have also been found
to produce FAS ligand, which may defend the tumor from
immune attack by triggering the apoptosis of lymphocytes.
The role of the immune system in the defense against cancer is
discussed in a later section.

during the infection and, after a few days, the activated T lym-
phocytes begin to produce another surface molecule called
FAS ligand. The binding of FAS to FAS ligand, on the same
or on different cells, triggers the apoptosis (cell suicide) of the
lymphocytes.
This mechanism also helps maintain certain parts of the
body—such as the inner region of the eye and the tubules of
the testis—as immunologically privileged sites. These sites
harbor molecules that the immune system would mistakenly
treat as foreign antigens if the site were not somehow pro-
tected. The Sertoli cells of the testicular tubules (chapter 20; see
fig. 20.16), for example, protect developing sperm from
immune attack through two mechanisms. First, the tight junc-
tions between adjacent Sertoli cells form a barrier that normally
prevents exposure of the immune system to the developing
sperm. Second, the Sertoli cells produce FAS ligand, which
triggers apoptosis of any T lymphocytes that may enter the area.
The anterior chamber of the eye is another immunologi-
cally privileged site. Immunological privilege here is ben-
eficial because any inflammation triggered by an immune
response could interfere with the transparency required for
vision or damage the neurological layers of the retina, which
cannot regenerate. It was long believed that antigens within the
anterior chamber of the eye were “hidden” from the immune
system, but more recent evidence suggests that immunological
privilege here involves more active processes. These include
coating of the interior of the eye with FAS ligand, which pro-
motes apoptosis of leukocytes, and the secretion of different
cytokines, which inhibit inflammation through a variety of
mechanisms.


CLINICAL APPLICATION
Glucocorticoid drugs —including hydrocortisone, cortisone,
prednisone, prednisolone, and dexamethasone —are used
to suppress the immune system for the treatment of various
inflammatory conditions, autoimmune diseases, and allergy.
Although they are broadly immunosuppressive, inhibiting
lymphocytes and phagocytic cells, they have been found to
enhance the cytokines secreted from T H 2 cells compared to
cytokines secreted from T H 1 cells, thereby promoting a shift
from cell-mediated to humoral immunity.
The immunosuppressive effects of glucocorticoids
result form their ability to suppress pro-inflammatory cyto-
kines, including IL-1 and other interleukins, gamma inter-
feron, and TNF a. However, these cytokines, released by
microglia in the brain, activate the pituitary-adrenal axis:
they stimulate the hypothalamus to secrete CRH, which
then stimulates the anterior pituitary to secrete ACTH and
thereby stimulate the adrenals to secrete cortisol (the glu-
cocorticoid hormone). Because a rise in glucocorticoids
suppresses the pro-inflammatory cytokines, a negative
feedback loop is completed. The nervous, endocrine, and
immune systems thereby interact with each other to main-
tain homeostasis.

| CHECKPOINT

6a. Describe the role of the thymus in cell-mediated
immunity, and identify the different types of
T lymphocytes.
6b. Define the term cytokines, state the origin of cytokine
molecules, and describe their different functions.
7a. Define the term histocompatibility antigens and
explain the importance of class-1 and class-2 MHC
molecules in the function of T cells.
7b. Describe the requirements for activation of helper
T cells by macrophages. Explain how helper T cells
promote the immunological defenses provided by
killer T cells and by B cells.

15.4 ACTIVE AND PASSIVE


IMMUNITY


When a person is first exposed to a pathogen, the immune
response may be insufficient to combat the disease. Dur-
ing the response, however, the lymphocytes that have
specificity for that antigen are stimulated to divide many
times and produce a clone. This is active immunity, and it
can protect the person from getting the disease upon sub-
sequent exposures.

LEARNING OUTCOMES

After studying this section, you should be able to:


  1. Explain how active immunity is produced, using the
    clonal selection theory.

  2. Explain how passive immunity is produced.


It first became known in Western Europe in the mid-eighteenth
century that the fatal effects of smallpox could be prevented by
inducing mild cases of the disease. This was accomplished at
that time by rubbing needles into the pustules of people who
had mild forms of smallpox and injecting these needles into
healthy people. Understandably, this method of immunization
did not gain wide acceptance.
Acting on the observation that milkmaids who contracted
cowpox—a disease similar to smallpox but less virulent (less
pathogenic)—were immune to smallpox, an English physician
named Edward Jenner inoculated a healthy boy with cowpox.
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