Tumor immunoevasion by the conversion of effector NK cells into type 1 innate lymphoid cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2017-09

AUTHORS

Yulong Gao, Fernando Souza-Fonseca-Guimaraes, Tobias Bald, Susanna S Ng, Arabella Young, Shin Foong Ngiow, Jai Rautela, Jasmin Straube, Nic Waddell, Stephen J Blake, Juming Yan, Laurent Bartholin, Jason S Lee, Eric Vivier, Kazuyoshi Takeda, Meriem Messaoudene, Laurence Zitvogel, Michele W L Teng, Gabrielle T Belz, Christian R Engwerda, Nicholas D Huntington, Kyohei Nakamura, Michael Hölzel, Mark J Smyth

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 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. More... »

PAGES

1004-1015

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.3800

DOI

http://dx.doi.org/10.1038/ni.3800

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1090931651

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28759001


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