The role of IFN-gamma in tumor transplantation immunity and inhibition of chemical carcinogenesis

Curr Opin Immunol. 2003 Apr;15(2):148-54. doi: 10.1016/s0952-7915(03)00007-4.


IFN-gamma contributes to the rejection of transplantable tumors and the inhibition of methylcholanthrene (MCA)-induced carcinogenesis by different mechanisms. In most tumor transplantation models, tumor rejection requires IFN-gamma receptor expression by host cells, but not by tumor cells. IFN-gamma produced by either CD4+ or CD8+ T cells acts on non-hematopoietic tumor stroma cells and, either directly or indirectly, induces angiostasis. This prevents rapid tumor burden and allows residual tumor cells to be eliminated. In some models, IFN-gamma also contributes to the destruction of existing tumor blood vessels. During MCA-induced tumorigenesis IFN-gamma is involved in the inhibition of MCA diffusion by encapsulation and reduction of DNA damage. This mechanism may primarily protect tissue from damage and simultaneously inhibit tumor development.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Carcinogens / administration & dosage
  • Graft Rejection / immunology*
  • Graft Rejection / metabolism
  • Graft Rejection / physiopathology
  • Humans
  • Interferon-gamma / immunology
  • Interferon-gamma / metabolism
  • Interferon-gamma / physiology*
  • Methylcholanthrene / administration & dosage
  • Neoplasm Transplantation / immunology
  • Neoplasms / chemically induced
  • Neoplasms / immunology
  • Neoplasms / physiopathology*


  • Carcinogens
  • Methylcholanthrene
  • Interferon-gamma