IFNγ and lymphocytes prevent primary tumour development and shape tumour immunogenicity

  title={IFN$\gamma$ and lymphocytes prevent primary tumour development and shape tumour immunogenicity},
  author={Vijay Shankaran and Hiroaki Ikeda and Allen T. Bruce and J. Michael White and Paul E. Swanson and Lloyd J. Old and Robert D. Schreiber},
Lymphocytes were originally thought to form the basis of a ‘cancer immunosurveillance’ process that protects immunocompetent hosts against primary tumour development, but this idea was largely abandoned when no differences in primary tumour development were found between athymic nude mice and syngeneic wild-type mice. However, subsequent observations that nude mice do not completely lack functional T cells and that two components of the immune system—IFNγ and perforin—help to prevent tumour… 
Sporadic immunogenic tumours avoid destruction by inducing T-cell tolerance
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Expression of tumour-specific antigens underlies cancer immunoediting
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Checkpoint Blockade Cancer Immunotherapy Targets Tumour-Specific Mutant Antigens
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IFN-γ is required for cytotoxic T cell-dependent cancer genome immunoediting
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Cancer immunoediting from immune surveillance to immune escape
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Memory T cells in cancer immunotherapy: which CD8 T-cell population provides the best protection against tumours?
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Immunotherapeutic potential of whole tumour cells
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Tumor-host immune interactions and dendritic cell dysfunction.


Perforin-Mediated Cytotoxicity Is Critical for Surveillance of Spontaneous Lymphoma
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Differential Tumor Surveillance by Natural Killer (Nk) and Nkt Cells
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Decreased tumor surveillance in perforin-deficient mice
Perforin-dependent cytotoxicity is not only a crucial mechanism of both cytotoxic T lymphocyte- and NK- dependent resistance to injected tumor cell lines, but also operates during viral and chemical carcinogenesis in vivo.
Demonstration of an interferon γ-dependent tumor surveillance system in immunocompetent mice
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Immune response in mice that lack the interferon-gamma receptor.
Mutant mice offer the possibility for the further elucidation of IFN-gamma-mediated functions by transgenic cell- or tissue-specific reconstitution of a functional receptor.
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Tissue-specific targeting of cytokine unresponsiveness in transgenic mice.
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