The immune surveillance theory was first conceptualized in the early 1900s by Paul Ehrlich. He suggested that cancer cells frequently arise in the body but are recognized as foreign and eliminated by the immune system. Some 50 years later, Lewis Thomas suggested that the cell-mediated branch of the immune system had evolved to patrol the body and eliminate cancer cells. According to these concepts, tumors arise only if cancer cells are able to escape immune surveillance, either by reducing their expression of tumor antigens or by an impairment in the immune response to these cells.
Among the early observations that seemed to support the immune surveillance theory was the increased incidence of cancer in transplantation patients on immunosuppressive drugs. Other findings, however, were difficult to reconcile with this theory. Nude mice, for example, lack a thymus and consequently lack functional T cells. According to the immune surveillance theory, these mice should show an increase in cancer, instead, nude mice are no more susceptible to cancer than other mice. Furthermore, although individuals on immunosuppressive drugs do show an increased incidence of cancers of the immune system, other common cancers (e.g., lung, breast, and colon cancer) are not increased in these individuals, contrary to what the theory predicts. One possible explanation for the selective increase in immune-system cancers is that the immunosuppressive agents themselves may exert a direct carcinogenic effect on immune cells.
Experimental data concerning the effect of tumor-cell dosage on the ability of the immune system to respond also are incompatible with the immune surveillance theory. For example, animals injected with very low or very high doses of tumor cells develop tumors, whereas those injected with intermediate doses do not. The mechanism by which a low dose of tumor cells "sneaks through" is difficult to reconcile with the immune surveillance theory. Finally, this theory assumes that cancer cells and normal cells exhibit qualitative antigen differences. In fact, as stated earlier, many types of tumors do not express tumor-specific antigens, and any immune response that develops must be induced by quantitative differences in antigen expression by normal cells and tumor cells. However, tumors induced by viruses would be expected to express some antigens encoded by the viral genome. These antigens are qualitatively different from those expressed by normal tissues and would be expected to attract the attention of the immune system. In fact, there are many examples of specific immune responses to virally induced tumors.
Nevertheless, apart from tumors caused by viruses, the basic concept of the immune surveillance theory—that malignant tumors arise only if the immune system is somehow impaired or if the tumor cells lose their immunogenicity, enabling them to escape immune surveillance—at this time remains unproved. In spite of this, it is clear that an immune response can be generated to tumor cells, and therapeutic approaches aimed at increasing that response may serve as a defense against malignant cells.
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