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

Official URL:https://doi.org/10.1016/S0952-7915(03)00007-4
PubMed:View item in PubMed
Creators Name:Blankenstein, T. and Qin, Z.H.
Journal Title:Current Opinion in Immunology
Journal Abbreviation:Curr Opin Immunol
Volume:15
Number:2
Page Range:148-154
Date:April 2003
Keywords:Carcinogens, Graft Rejection, Interferon Type II, Methylcholanthrene, Neoplasm Transplantation, Neoplasms, Animals
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.
ISSN:0952-7915
Publisher:Current Biology Ltd (England)
Item Type:Review

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