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The immunoreceptor NKG2D promotes tumour growth in a model of hepatocellular carcinoma

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Listed:
  • Sam Sheppard

    (Imperial College London)

  • Joana Guedes

    (Imperial College London)

  • Anna Mroz

    (Imperial College London)

  • Anastasia-Maria Zavitsanou

    (Imperial College London)

  • Hiromi Kudo

    (Imperial College London)

  • Stephen M. Rothery

    (Facility for Imaging by Light Microscopy, Imperial College London)

  • Panagiotis Angelopoulos

    (National Technical University of Athens)

  • Robert Goldin

    (Imperial College London)

  • Nadia Guerra

    (Imperial College London)

Abstract

Inflammation is recognized as one of the drivers of cancer. Yet, the individual immune components that possess pro- and anti-tumorigenic functions in individual cancers remain largely unknown. NKG2D is a potent activating immunoreceptor that has emerged as an important player in inflammatory disorders besides its well-established function as tumour suppressor. Here, we provide genetic evidence of an unexpected tumour-promoting effect of NKG2D in a model of inflammation-driven liver cancer. Compared to NKG2D-deficient mice, NKG2D-sufficient mice display accelerated tumour growth associated with, an increased recruitment of memory CD8+T cells to the liver and exacerbated pro-inflammatory milieu. In addition, we show that NKG2D contributes to liver damage and consequent hepatocyte proliferation known to favour tumorigenesis. Thus, the NKG2D/NKG2D-ligand pathway provides an additional mechanism linking chronic inflammation to tumour development in hepatocellular carcinoma. Our findings expose the need to selectively target the types of cancer that could benefit from NKG2D-based immunotherapy.

Suggested Citation

  • Sam Sheppard & Joana Guedes & Anna Mroz & Anastasia-Maria Zavitsanou & Hiromi Kudo & Stephen M. Rothery & Panagiotis Angelopoulos & Robert Goldin & Nadia Guerra, 2017. "The immunoreceptor NKG2D promotes tumour growth in a model of hepatocellular carcinoma," Nature Communications, Nature, vol. 8(1), pages 1-13, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms13930
    DOI: 10.1038/ncomms13930
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