title: The role of IFN-gamma in tumor transplantation immunity and inhibition of chemical carcinogenesis.
abstract: 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.
authors.affiliation: Max-Delbrück Center for Molecular Medicine, 13092 Berlin, Germany. tblanke@mdc-berlin.de
authors.forename: Thomas
authors.initials: T
authors.lastname: Blankenstein
authors.forename: Zhihai
authors.initials: Z
authors.lastname: Qin
mesh_terms: D000818:Animals; D002273:Carcinogens / Q000008:administration & dosage; D006084:Graft Rejection / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism / Q000502:physiology*; D008748:Methylcholanthrene / Q000008:administration & dosage; D009368:Neoplasm Transplantation / Q000276:immunology; D009369:Neoplasms / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology*
chemical_list: D002273:Carcinogens; D008748:Methylcholanthrene; D007371:Interferon-gamma