Immune surveillance--a powerful mechanism with a limited range

Abstract

There is excellent evidence for the belief that immune surveillance mechanisms prevent the outgrowth of potentially neoplastic cells induced by horizontally transmitted, ubiquitous, potentially oncogenic viruses, indigenous to natural populations. Polyoma virus in mice, Marek's disease in the chicken, Herpesvirus saimiri in the squirrel monkey, and the Epstein-Barr virus in man are examples. There is much less evidence for immune surveillance against chemically induced tumors. It is argued that surveillance against the virus-induced tumors may have evolved by the selective fixation of appropriate immune responsiveness (IR) genes. It is important to distinguish between the breakdown of an existing surveillance mechanism, e.g., by immunosuppresion, and the lack of immune recognition, due to the deficiency of the IR gene equipment. Presently available in vitro lymphocytotoxicity tests are not yet developed to the point where they can reliably distinguish between these alternatives.