The Immune System 51915.5 TUMOR IMMUNOLOGY
Tumor cells can reveal antigens that stimulate the destruc-
tion of the tumor. When cancers develop, this immuno-
logical surveillance system—primarily the function of T cells
and natural killer cells—has failed to prevent the growth and
metastasis of the tumor.
LEARNING OUTCOMES
After studying this section, you should be able to:- Explain the relationship between the immune system
and cancer.
Characteristic Active Immunity Passive Immunity
Injection of person with Antigens Antibodies
Source of antibodies The person inoculated Natural—the mother; artificial—injection with antibodies
Method Injection with killed or attenuated pathogens
or their toxinsNatural—transfer of antibodies across the placenta;
artificial—injection with antibodies
Time to develop resistance 5 to 14 days Immediately after injection
Duration of resistance Long (perhaps years) Short (days to weeks)
When used Before exposure to pathogen Before or after exposure to pathogenTable 15.9 | Comparison of Active and Passive Immunity
Oncology (the study of tumors) has revealed that tumor biol-
ogy is similar to and interrelated with the functions of the
immune system. Most tumors appear to be clones of single
cells that have become transformed in a process similar to the
development of lymphocyte clones in response to specific anti-
gens. Lymphocyte clones, however, are under complex inhibi-
tory control systems—such as those exerted by regulatory
T lymphocytes and negative feedback by antibodies. The divi-
sion of tumor cells, by contrast, is not effectively controlled by
normal inhibitory mechanisms. Tumor cells are also relatively
unspecialized—they dedifferentiate, which means that they
become similar to the less specialized cells of an embryo.
Tumors are described as benign when they are relatively
slow growing and limited to a specific location (warts, for
example). Malignant tumors grow more rapidly and undergo
metastasis, a term that refers to the dispersion of tumor cells
and the resultant seeding of new tumors in different loca-
tions. The term cancer, as it is generally applied, refers to
malignant tumors. The word cancer (Latin for “crab”) stems
from Hippocrates’ observation of a tumor being fed by blood
vessels, which resembled the claws of a crab. Cancer is now
believed to result from altered expression of oncogenes
(genes that promote cancer), tumor-suppressor genes,
and genes that code for microRNA (miRNA; chapter 3,
section 3.3).
As tumor cells dedifferentiate, they reveal surface anti-
gens that can stimulate the immune destruction of the tumor.
Consistent with the concept of dedifferentiation, some of
these antigens are proteins produced in embryonic or fetal
life and not normally produced postnatally. Because they are
absent at the time immunological competence is established,
they are treated as foreign and fit subjects for immunologi-
cal attack when they are produced by cancerous cells. The
release of two such antigens into the blood has provided the
basis for laboratory diagnosis of some cancers. Carcinoem-
bryonic antigen tests are useful in the diagnosis of colon can-
cer, for example, and tests for alpha-fetoprotein (normally
produced only by the fetal liver) help in the diagnosis of liver
cancer.
The immune system can guard against cancer by recog-
nizing antigens that are expressed in malignantly transformed
cells. For example, carcinogens cause mutations, and these
mutated genes can produce tumor-specific antigens. Also,
some cancers are caused by viruses and so can display viral
antigens that flag tumor cells. Examples include antigens of
the human papillomavirus, which can cause cervical can-
cer, and antigens of the Epstein-Barr virus, which can cause
Burkitt’s lymphoma and nasopharyngeal carcinoma. Even
normal self-antigens, if they are overexpressed due to gene
duplication, may trigger attack by the adaptive immune sys-
tem. In cases where tumor cells do not display antigens that
directly stimulate T and B lymphocytes, the tumor cells may
still activate the natural killer (NK) cells (discussed next) of
the innate immune system. The adaptive immune response
could then be triggered by molecules generated during the
inflammation caused by the innate immune response to the
tumor cells.
Tumor antigens activate the immune system, initiating an
attack primarily by killer T lymphocytes ( fig. 15.22 ) and natu-
ral killer cells (described in the next section). The concept of
immunological surveillance against cancer was introduced in