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IFNγ and lymphocytes prevent primary tumour development and shape tumour immunogenicity

Author

Listed:
  • Vijay Shankaran

    (Center for Immunology, Washington University School of Medicine)

  • Hiroaki Ikeda

    (Center for Immunology, Washington University School of Medicine)

  • Allen T. Bruce

    (Center for Immunology, Washington University School of Medicine)

  • J. Michael White

    (Center for Immunology, Washington University School of Medicine)

  • Paul E. Swanson

    (Center for Immunology, Washington University School of Medicine)

  • Lloyd J. Old

    (Ludwig Institute for Cancer Research, New York Branch at Memorial Sloan-Kettering Cancer Center)

  • Robert D. Schreiber

    (Center for Immunology, Washington University School of Medicine)

Abstract

Lymphocytes were originally thought to form the basis of a ‘cancer immunosurveillance’ process that protects immunocompetent hosts against primary tumour development1,2, but this idea was largely abandoned when no differences in primary tumour development were found between athymic nude mice and syngeneic wild-type mice3,4,5. However, subsequent observations that nude mice do not completely lack functional T cells6,7 and that two components of the immune system—IFNγ8,9 and perforin10,11,12—help to prevent tumour formation in mice have led to renewed interest in a tumour-suppressor role for the immune response. Here we show that lymphocytes and IFNγ collaborate to protect against development of carcinogen-induced sarcomas and spontaneous epithelial carcinomas and also to select for tumour cells with reduced immunogenicity. The immune response thus functions as an effective extrinsic tumour-suppressor system. However, this process also leads to the immunoselection of tumour cells that are more capable of surviving in an immunocompetent host, which explains the apparent paradox of tumour formation in immunologically intact individuals.

Suggested Citation

  • Vijay Shankaran & Hiroaki Ikeda & Allen T. Bruce & J. Michael White & Paul E. Swanson & Lloyd J. Old & Robert D. Schreiber, 2001. "IFNγ and lymphocytes prevent primary tumour development and shape tumour immunogenicity," Nature, Nature, vol. 410(6832), pages 1107-1111, April.
  • Handle: RePEc:nat:nature:v:410:y:2001:i:6832:d:10.1038_35074122
    DOI: 10.1038/35074122
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    Cited by:

    1. Alexander Piening & Emily Ebert & Carter Gottlieb & Niloufar Khojandi & Lindsey M. Kuehm & Stella G. Hoft & Kelly D. Pyles & Kyle S. McCommis & Richard J. DiPaolo & Stephen T. Ferris & Elise Alspach &, 2024. "Obesity-related T cell dysfunction impairs immunosurveillance and increases cancer risk," Nature Communications, Nature, vol. 15(1), pages 1-12, December.
    2. Chun Wai Wong & Christos Evangelou & Kieran N. Sefton & Rotem Leshem & Wei Zhang & Vishaka Gopalan & Sorayut Chattrakarn & Macarena Lucia Fernandez Carro & Erez Uzuner & Holly Mole & Daniel J. Wilcock, 2023. "PARP14 inhibition restores PD-1 immune checkpoint inhibitor response following IFNγ-driven acquired resistance in preclinical cancer models," Nature Communications, Nature, vol. 14(1), pages 1-21, December.
    3. Heng-Jia Liu & Heng Du & Damir Khabibullin & Mahsa Zarei & Kevin Wei & Gordon J. Freeman & David J. Kwiatkowski & Elizabeth P. Henske, 2023. "mTORC1 upregulates B7-H3/CD276 to inhibit antitumor T cells and drive tumor immune evasion," Nature Communications, Nature, vol. 14(1), pages 1-22, December.
    4. Yazhong Cui & Yang Miao & Longzhi Cao & Lifang Guo & Yue Cui & Chuanzhe Yan & Zhi Zeng & Mo Xu & Ting Han, 2023. "Activation of melanocortin-1 receptor signaling in melanoma cells impairs T cell infiltration to dampen antitumor immunity," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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