Dataset related to article "Neutrophils Driving Unconventional T Cells Mediate Resistance against Murine Sarcomas and Selected Human Tumors"
- 1. Humanitas Clinical and Research Center – IRCCS -, via Manzoni 56, 20089 Rozzano (Mi) - Italy
- 2. Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
- 3. Humanitas Clinical and Research Center – IRCCS -, via Manzoni 56, 20089 Rozzano (Mi) - Italy AND Humanitas University, Department of Biomedical Sciences, Via Rita Levi Montalcini 4, 20090 Pieve Emanuele – Milan, Italy
- 4. Pathology Department, Fondazione IRCCS Istituto Nazionale Tumori, 20133 Milan, Italy.
- 5. Zoology Department College of Science, King Saud University, 12372 Riyadh, Saudi Arabia.
- 6. Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park SK10 4GT, UK.
- 7. Department of Translational Medical Sciences and Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, 80138 Naples, Italy.
Description
Neutrophils are a component of the tumor microenvironment and have been predominantly associated with cancer progression. Using a genetic approach complemented by adoptive transfer, we found that neutrophils are essential for resistance against primary 3-methylcholantrene-induced carcinogenesis. Neutrophils were essential for the activation of an interferon-γ-dependent pathway of immune resistance, associated with polarization of a subset of CD4- CD8- unconventional αβ T cells (UTCαβ). Bulk and single-cell RNA sequencing (scRNA-seq) analyses unveiled the innate-like features and diversity of UTCαβ associated with neutrophil-dependent anti-sarcoma immunity. In selected human tumors, including undifferentiated pleomorphic sarcoma, CSF3R expression, a neutrophil signature and neutrophil infiltration were associated with a type 1 immune response and better clinical outcome. Thus, neutrophils driving UTCαβ polarization and type 1 immunity are essential for resistance against murine sarcomas and selected human tumors.
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Additional details
Related works
- Is supplement to
- Journal article: 31257026 (PMID)
- Journal article: 10.1016/j.cell.2019.05.047 (DOI)