637
CHAPTER SIXTEEN
Lymphatic System and Immunity
memory B cells with memory T cells produce a
secondary
immune response.
In lymph nodes,
follicular dendritic cells
may help memory by harboring and slowly releasing viral
antigens after an initial infection. This constantly stimulates
memory B cells, which present the antigens to memory T
cells, maintaining immunity.
As a result of a primary immune response, detectable
concentrations of antibodies usually appear in the plasma
within five to ten days after exposure to antigens. If the
identical antigen is encountered later, a secondary immune
response may produce additional antibodies within a day
or two
(f
g. 16.21)
. Although newly formed antibodies may
persist in the body for only a few months or years, memory
cells live much longer. A secondary immune response may
be very long-lasting.
Immune Responses
When B cells or T cells become activated after F
rst encoun-
tering the antigens for which they are specialized to react,
their actions constitute a
primary immune response.
During
such a response, plasma cells release antibodies (IgM, fol-
lowed by IgG) into the lymph. The antibodies are transported
to the blood and then throughout the body, where they help
destroy antigen-bearing agents. Production and release of
antibodies continues for several weeks.
After a primary immune response, some of the B cells
produced during proliferation of the clone remain dormant
and serve as
memory cells
(see F g. 16.19). If the identical
antigen is encountered in the future, the clones of these mem-
ory cells enlarge, and they can respond rapidly with IgG to
the antigen to which they were previously sensitized. These
chorionic gonadotropin (see chapter 23, p. 882),
indicating pregnancy.
MAbs can highlight a new cancer or detect
recurrence. The MAb is attached to a radioactive
chemical, which emits a signal when the MAb
binds an antigen unique to the cancer cell surface.
MAbs can ferry conventional cancer treat-
ments to where they are needed and spare
healthy tissue. Drugs or radioactive chemicals are
attached to MAbs that deliver them to antigens
on cancer cells. When injected into a patient, the
MAb and its cargo are engulfed by the cancer
cells, which are destroyed. MAbs can also combat
cancer directly by blocking growth factors that
otherwise bind cancer cells, stimulating them to
divide. Table 16A lists some MAb-based drugs and
how they work. They have rare adverse effects,
including anaphylactic shock and severe anemia.
Cytokines
Immunotherapy experiments were difficult to
do in the late 1960s because cytokines and anti-
bodies could be obtained only in small amounts
from cadavers. In the 1970s, recombinant DNA
and monoclonal antibody technologies yielded
unlimited amounts of pure proteins—just as the
AIDS epidemic was making it essential to F
nd a
purer source of biochemicals than cadavers.
Interferon was the first cytokine tested on a
large scale. It is used to treat a dozen or so condi-
tions, including a type of leukemia, multiple scle-
rosis, hepatitis, and genital warts. Interleukin-2 is
used to treat kidney cancer, and colony-stimulating
factors boost the white blood cell supply in peo-
ple whose immune systems are temporarily sup-
pressed, such as those receiving drugs to treat
cancer or AIDS, or transplant recipients.
Increasingly, cancer treatment consists of
combinations of immune system cells or biochem-
icals, plus standard therapies. Immunotherapy
can enable a patient to withstand higher doses
of a conventional drug or destroy cancer cells
remaining after standard treatment.
TABLE
16A
|
Drugs Based on Monoclonal Antibodies
Drug
Condition
Mechanism
Tysabri
Multiple sclerosis
Binds cells that produce autoantibodies against brain
and/or spinal cord tissue
Erbitux
Colorectal cancer
Blocks growth factor receptor overabundant on cancer
cells, preventing cell division
Herceptin
Breast cancer
Blocks growth factor receptor overabundant on cancer
cells, preventing cell division
Iressa
Lung cancer
Blocks growth factor receptor overabundant on cancer
cells, preventing cell division
Avastin
Colorectal cancer
Lung cancer
Blocks growth factor from stimulating formation of
blood vessels to tumor
Raptiva
Psoriasis
Blocks T cell functions
Xolair
Asthma
Blocks IgE, preventing allergic response
Synagis
Respiratory syncytial virus
infection
Binds virus part required to enter cells
Remicade
Crohn disease
Rheumatoid arthritis
Blocks excess tumor necrosis factor
Rituxan
B cell lymphoma
Blocks CD20 protein receptor on all B cells—
bone marrow stem cells then restore healthy B cells
Zenapax
Rejection of transplant
Blocks IL-2 from rejecting transplant
previous page 667 David Shier Hole's Human Anatomy and Physiology 2010 read online next page 669 David Shier Hole's Human Anatomy and Physiology 2010 read online Home Toggle text on/off