Cytokine-based transformation of immune surveillance into tumor-promoting inflammation

Oncogene. 2008 Oct 6;27(45):5913-9. doi: 10.1038/onc.2008.275.


During the last decade, it has become clear that the mammalian immune system is able to recognize and partially suppress nascent tumors. Human T cells specific to oncogenes and onco-fetal antigens are present in human cancer patients and their tumors. At the same time, molecular links between tumor-associated inflammation and tumor progression have been uncovered, providing an explanation for the long recognized epidemiological link between inflammation and cancer. The synopsis of these findings suggests a new interpretation of tumor immunity. It appears that antigen recognition or antigen-specific T-cell expansion at large is not as profoundly impaired in tumor patients as the correct polarization, the survival and the effector function of tumor-infiltrating T cells. This review will focus on pro-inflammatory cytokines likely to contribute to the deregulation of tumor-specific immunity and its consequences.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Proliferation / drug effects
  • Cytokines / adverse effects*
  • Cytokines / physiology
  • Humans
  • Immunologic Surveillance / physiology*
  • Inflammation / complications*
  • Inflammation / immunology
  • Interleukin-12 / physiology
  • Interleukin-23 / physiology
  • Interleukin-6 / adverse effects
  • Interleukin-6 / pharmacology
  • Interleukin-6 / physiology
  • Models, Biological
  • Neoplasms / etiology*
  • Neoplasms / immunology
  • Neoplasms / pathology
  • Transforming Growth Factor beta / physiology
  • Tumor Necrosis Factor-alpha / adverse effects
  • Tumor Necrosis Factor-alpha / physiology


  • Cytokines
  • Interleukin-23
  • Interleukin-6
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Interleukin-12