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

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