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A cancer immunosurveillance controversy

Nature Immunology volume 5, pages 3–4 (2004)Cite this article

To the editor:

Recently, the idea of T cell–mediated cancer immune surveillance against chemically induced and spontaneous cancer was revived1, based on studies showing that mice lacking IFN-γ, IFN-γ-receptor (IFN-γR), IFN-γ-producing cell types or perforin have increased tumor susceptibility to 3-methylcholanthrene (MCA) and a high tumor incidence in aged mice deficient in recombination activation gene 2 (RAG-2). All further experiments were based on tumor transplantation. It is unlikely that rejection of transplanted tumor cells, typically mediated by T cells, and inhibition of MCA carcinogenesis involve the same mechanism. We suggest that a 'tissue repair' response, during which MCA is encapsulated2, may mediate protection. In contrast to immune surveillance, a tissue repair response does not involve T cells. It is suspicious that regardless which IFN-γ producers (αβ+, δγ+ or all T cells; natural killer or natural killer T cells) are lacking, mice have increased susceptibility to MCA1. This indicates that either all these cells are active participants during tumor elimination1 or steady-state IFN-γ concentrations are different between the knockout and control mice. In most of the studies mentioned above1 the immune-deficient mice were bred locally and control mice were purchased. The transfer of mice to a new environment or a local T cell response induces widespread IFN-γ-dependent major histocompatibility complex expression in remote organs3,4. Therefore, exposure of mice to a new environment with differences in flora, food, air and water would probably influence the immune status and increase IFN-γ production. This could nonspecifically contribute to the protective response against MCA. Thus, use of non-littermates, the transfer of mice to a new environment or unknown environmental factors in animal facilities could increase IFN-γ production by control mice in a manner unrelated to the experimental treatment.

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Figure 1: RAG-1- and perforin-deficient mice have tumor incidence similar to that of wild-type mice after injection of MCA.

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Authors and Affiliations

  1. Institute of Immunology, Free University Berlin, Berlin, 12200, Germany

    Zhihai Qin & Thomas Blankenstein

  2. Max-Delbrück-Centrum for Molecular Medicine, Berlin, 13092, Germany

    Thomas Blankenstein

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  1. Zhihai Qin
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  2. Thomas Blankenstein
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Qin, Z., Blankenstein, T. A cancer immunosurveillance controversy. Nat Immunol 5, 3–4 (2004). https://doi.org/10.1038/ni0104-3

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