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  • Tumor immunoevasion by the conversion of effector NK cells into type 1 innate lymphoid cells

    Author(s)
    Gao, Yulong
    Souza-Fonseca-Guimaraes, Fernando
    Bald, Tobias
    Ng, Susanna S
    Young, Arabella
    Ngiow, Shin Foong
    Rautela, Jai
    Straube, Jasmin
    Waddell, Nic
    Blake, Stephen J
    Yan, Juming
    Bartholin, Laurent
    Lee, Jason S
    Vivier, Eric
    Takeda, Kazuyoshi
    Messaoudene, Meriem
    Zitvogel-, Laurence
    Teng, Michele WL
    Belz, Gabrielle T
    Engwerda, Christian R
    Huntington, Nicholas D
    Nakamura, Kyohei
    Hoelzel, Michael
    Smyth, Mark J
    Griffith University Author(s)
    Ng, Susanna SS.
    Engwerda, Christian R.
    Year published
    2017
    Metadata
    Show full item record
    Abstract
    Avoiding destruction by immune cells is a hallmark of cancer, yet how tumors ultimately evade control by natural killer (NK) cells remains incompletely defined. Using global transcriptomic and flow-cytometry analyses and genetically engineered mouse models, we identified the cytokine-TGF-β-signaling-dependent conversion of NK cells (CD49a−CD49b+Eomes+) into intermediate type 1 innate lymphoid cell (intILC1) (CD49a+CD49b+Eomes+) populations and ILC1 (CD49a+CD49b−Eomesint) populations in the tumor microenvironment. Strikingly, intILC1s and ILC1s were unable to control local tumor growth and metastasis, whereas NK cells favored ...
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    Avoiding destruction by immune cells is a hallmark of cancer, yet how tumors ultimately evade control by natural killer (NK) cells remains incompletely defined. Using global transcriptomic and flow-cytometry analyses and genetically engineered mouse models, we identified the cytokine-TGF-β-signaling-dependent conversion of NK cells (CD49a−CD49b+Eomes+) into intermediate type 1 innate lymphoid cell (intILC1) (CD49a+CD49b+Eomes+) populations and ILC1 (CD49a+CD49b−Eomesint) populations in the tumor microenvironment. Strikingly, intILC1s and ILC1s were unable to control local tumor growth and metastasis, whereas NK cells favored tumor immunosurveillance. Experiments with an antibody that neutralizes the cytokine TNF suggested that escape from the innate immune system was partially mediated by TNF-producing ILC1s. Our findings provide new insight into the plasticity of group 1 ILCs in the tumor microenvironment and suggest that the TGF-β-driven conversion of NK cells into ILC1s is a previously unknown mechanism by which tumors escape surveillance by the innate immune system.
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    Journal Title
    Nature Immunology
    Volume
    18
    Issue
    9
    DOI
    https://doi.org/10.1038/ni.3800
    Subject
    Immunology
    Cellular immunology
    Innate immunity
    Publication URI
    http://hdl.handle.net/10072/353986
    Collection
    • Journal articles

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