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Cell. 2016 Jan 28;164(3):365-77. doi: 10.1016/j.cell.2016.01.002. Epub 2016 Jan 21.

Cancer Immunosurveillance by Tissue-Resident Innate Lymphoid Cells and Innate-like T Cells.

Author information

1
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
2
Computational Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Physiology Biophysics and Systems Biology Graduate Program, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA.
3
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Computational Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Biochemistry & Structural Biology, Cell & Developmental Biology, and Molecular Biology Program, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA.
4
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Immunology and Microbial Pathogenesis Graduate Program, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA.
5
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Louis V. Gerstner Jr. Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
6
Computational Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
7
Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: lim@mskcc.org.

Abstract

Malignancy can be suppressed by the immune system in a process termed immunosurveillance. However, to what extent immunosurveillance occurs in spontaneous cancers and the composition of participating cell types remains obscure. Here, we show that cell transformation triggers a tissue-resident lymphocyte response in oncogene-induced murine cancer models. Non-circulating cytotoxic lymphocytes, derived from innate, T cell receptor (TCR)αβ, and TCRγδ lineages, expand in early tumors. Characterized by high expression of NK1.1, CD49a, and CD103, these cells share a gene-expression signature distinct from those of conventional NK cells, T cells, and invariant NKT cells. Generation of these lymphocytes is dependent on the cytokine IL-15, but not the transcription factor Nfil3 that is required for the differentiation of tumor-infiltrating NK cells, and IL-15 deficiency, but not Nfil3 deficiency, results in accelerated tumor growth. These findings reveal a tumor-elicited immunosurveillance mechanism that engages unconventional type-1-like innate lymphoid cells and type 1 innate-like T cells.

PMID:
26806130
PMCID:
PMC4733424
DOI:
10.1016/j.cell.2016.01.002
[Indexed for MEDLINE]
Free PMC Article

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