期刊
CELL
卷 175, 期 4, 页码 1014-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2018.09.030
关键词
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资金
- National Cancer Institute of the National Institutes of Health [RO1CA190700]
- Parker Institute for Cancer Immunotherapy, the Cancer Research Institute
- Janssen Pharmaceutical Company of Johnson and Johnson
- Prostate Cancer Foundation
- Stand Up To Cancer Lustgarten Foundation Pancreatic Cancer Convergence Dream Team Translational Research Grant
- Cancer Research Institute
- Government of Russian Federation [08-08]
- National Cancer Institute of the National Institutes of Health Paul Calabresi Career Development Award in Clinical Oncology [K12CA167540]
- Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs
- National Cancer Institute of the National Institutes of Health Cancer Center Support Grant [P30CA91842]
Although current immune-checkpoint therapy (ICT) mainly targets lymphoid cells, it is associated with a broader remodeling of the tumor micro-environment. Here, using complementary forms of high-dimensional profiling, we define differences across all hematopoietic cells from syngeneic mouse tumors during unrestrained tumor growth or effective ICT. Unbiased assessment of gene expression of tumor-infiltrating cells by single-cell RNA sequencing (scRNAseq) and longitudinal assessment of cellular protein expression by mass cytometry (CyTOF) revealed significant remodeling of both the lymphoid and myeloid intratumoral compartments. Surprisingly, we observed multiple subpopulations of monocytes/macrophages, distinguishable by the markers CD206, CX3CR1, CD1d, and iNOS, that change over time during ICT in a manner partially dependent on IFN gamma. Our data support the hypothesis that this macrophage polarization/activation results from effects on circulatory monocytes and early macrophages entering tumors, rather than on pre-polarized mature intratumoral macrophages.
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