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    NKG2D fine-tunes the local inflammatory response in colorectal cancer

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    Authors
    Curio, S.
    Lin, W.
    Bromley, Christian
    McGovern, J.
    Triulzi, C.
    Jonsson, G.
    Ghislat, G.
    Zelenay, Santiago
    Guerra, N.
    Affiliation
    Department of Life Sciences, Imperial College London, London SW7 2BX, UK
    Issue Date
    2023
    
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    Abstract
    Treating colorectal cancer (CRC) is a major challenge due to the heterogeneous immunological, clinical and pathological landscapes. Immunotherapy has so far only proven effective in a very limited subgroup of CRC patients. To better define the immune landscape, we examined the immune gene expression profile in various subsets of CRC patients and used a mouse model of intestinal tumors to dissect immune functions. We found that the NK cell receptor, natural-killer group 2 member D (NKG2D, encoded by KLRK1) and NKG2D ligand gene expression is elevated in the most immunogenic subset of CRC patients. High level of KLRK1 positively correlated with the mRNA expression of IFNG and associated with a poor survival of CRC patients. We further show that NKG2D deficiency in the Apcmin/+ mouse model of intestinal tumorigenesis led to reduced intratumoral IFNγ production, reduced tumorigenesis and enhanced survival, suggesting that the high levels of IFNγ observed in the tumors of CRC patients may be a consequence of NKG2D engagement. The mechanisms governing the contribution of NKG2D to CRC progression highlighted in this study will fuel discussions about (i) the benefit of targeting NKG2D in CRC patients and (ii) the need to define the predictive value of NKG2D and NKG2D ligand expression across tumor types.
    Citation
    Curio S, Lin W, Bromley C, McGovern J, Triulzi C, Jonsson G, et al. NKG2D Fine-Tunes the Local Inflammatory Response in Colorectal Cancer. Cancers (Basel). 2023 Mar 16;15(6). PubMed PMID: 36980678. Pubmed Central PMCID: PMC10046042. Epub 2023/03/30. eng.
    Journal
    Cancers
    URI
    http://hdl.handle.net/10541/626181
    DOI
    10.3390/cancers15061792
    PubMed ID
    36980678
    Additional Links
    https://dx.doi.org/10.3390/cancers15061792
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.3390/cancers15061792
    Scopus Count
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    All Paterson Institute for Cancer Research

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