IMR Press / FBS / Volume 2 / Issue 3 / DOI: 10.2741/S126

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

To suppress to rescue? Changing the approach for recalling anticancer immune responses
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1 Laboratory of Natural Cell Immunity, Department of Immunology and Gnotobiology, Institute of Microbiology, Academy of Sciences of the Czech Republic, vvi, Prague, Czech Republic
2 Laboratory of Tumor Biology, Department of Animal Embryology and Differentiation of Cells and Tissues, Institute of Animal Physiology and Genetics, Academy of Sciences of the Czech Republic, v.v.i., Libechov, Czech Republic

*Author to whom correspondence should be addressed.


Front. Biosci. (Schol Ed) 2010, 2(3), 1189–1197;
Published: 1 June 2010

The tumor microenvironment plays a fundamental role in both the organization of and the escape from anticancer immune response. Recent experimental approaches in anticancer therapy show that some anticancer chemotherapeutics--at a different dosage than usually used--can improve tumor control by acting on immunity and can also be used in immunosuppressive treatments. These apparently contrasting effects may provide an explanation by looking at the cancer immunity from a different perspective. Basing our hypothesis on the current inflammatory cancer microenvironment model, we suggest that the tumor escape may derive from a conflict between a deregulated local immune response and the application by the systemic immunity of a homeostatic regulation, physiologically used for terminating inflammatory processes. This regulation applied to the tumor microenvironment can contribute to impede the efficacy of anticancer responses. Therefore, we suggest recovering the anticancer response by paradoxically inducing a temporary immune suppression ("resetting" effect). In this paper, we review present concepts about inflammation and immunity in the cancer microenvironment, as well as experimental data from recent literature supporting this paradoxical intervention hypothesis.

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