Beginnings of the Immune Surveillance Theory

In the early 1900s, Ehrlich [1] proposed that a critical function of the immune system was to detect and eliminate carcinomas from the host. Thomas [2] and Burnet [3] developed the theory of immune surveillance proposing that tumor cells developed frequently and expressed tumor antigens that triggered the host to generate an immune-mediated response that eliminated the tumor. Studies by Old and Boyse [4] and Klein [5] in the 1960s confirmed the existence of tumor antigens on chemically or virally transformed murine tumors, and observed that tumors expressing these antigens were rapidly eliminated in syngeneic hosts. If the theory of immune surveillance was correct, then there would be an increase in spontaneous tumor incidence in immunocompromised hosts compared to tumor incidence in immunocompetent hosts. However, tumor studies in nude mice that lack functional T and B cells demonstrated no changes in the incidence of spontaneous tumor development compared to immunocompetent hosts [6]. Supporters of the immune surveillance theory argued that nude mice were not completely immunodeficient, since nude mice, while defective in T cell immunity, still possessed an intact innate immune response that may be critical in immune surveillance [7]. Even though this argument proved much later to be correct, at the time, there were no experimental models that could rigorously test the role of innate immunity in immune surveillance, and in the absence of data, the theory quickly lost favor among immunologists.

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