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.
journal_name
Celljournal_title
Cellauthors
Dadi S,Chhangawala S,Whitlock BM,Franklin RA,Luo CT,Oh SA,Toure A,Pritykin Y,Huse M,Leslie CS,Li MOdoi
10.1016/j.cell.2016.01.002subject
Has Abstractpub_date
2016-01-28 00:00:00pages
365-77issue
3eissn
0092-8674issn
1097-4172pii
S0092-8674(16)00003-9journal_volume
164pub_type
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