免疫监视
生物
先天性淋巴细胞
细胞毒性T细胞
免疫学
先天免疫系统
细胞生物学
自然杀伤性T细胞
免疫系统
CD8型
癌症研究
遗传学
体外
作者
Saïda Dadi,Sagar Chhangawala,Benjamin M. Whitlock,Ruth A. Franklin,Chong Luo,Soyoung Oh,Ahmed Toure,Yuri Pritykin,Morgan Huse,Christina Leslie,Ming O. Li
出处
期刊:Cell
[Elsevier]
日期:2016-01-01
卷期号:164 (3): 365-377
被引量:264
标识
DOI:10.1016/j.cell.2016.01.002
摘要
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.
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