The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Myeloid cells are required for PD-1/PD-L1 checkpoint activation and the establishment of an immunosuppressive environment in pancreatic cancer
Open accessAbstract
Background: Pancreatic cancer is characterised by the accumulation of a fibro-inflammatory stroma. Within this stromal reaction, myeloid cells are a predominant population. Distinct myeloid subsets have been correlated with tumour promotion and unmasking of anti-tumour immunity. Objective: The goal of this study was to determine the effect of myeloid cell depletion on the onset and progression of pancreatic cancer and to understand the relationship between myeloid cells and T cell-mediated immunity within the pancreatic cancer microenvironment. Methods: Primary mouse pancreatic cancer cells were transplanted into CD11b-diphtheria toxin receptor (DTR) mice. Alternatively, the iKras* mouse model of pancreatic cancer was crossed into CD11b-DTR mice. CD11b+ cells (mostly myeloid cell population) were depleted by diphtheria toxin treatment during tumour initiation or in established tumours. Results: Depletion of myeloid cells prevented Kras G12D-driven pancreatic cancer initiation. In pre-established tumours, myeloid cell depletion arrested tumour growth and in some cases, induced tumour regressions that were dependent on CD8+ T cells. We found that myeloid cells inhibited CD8+ T-cell anti-tumour activity by inducing the expression of programmed cell death-ligand 1 (PD-L1) in tumour cells in an epidermal growth factor receptor (EGFR)/mitogen-activated protein kinases (MAPK)-dependent manner. Conclusion: Our results show that myeloid cells support immune evasion in pancreatic cancer through EGFR/MAPK-dependent regulation of PD-L1 expression on tumour cells. Derailing this crosstalk between myeloid cells and tumour cells is sufficient to restore anti-tumour immunity mediated by CD8+ T cells, a finding with implications for the design of immune therapies for pancreatic cancer.
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Cites
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Self-citationOncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice
Collins, M. A., Bednar, F., Zhang, Y., Brisset, J.-C., Galbán, S., Galbán, C. J., Rakshit, S., Flannagan, K. S., Adsay, N. V., & Pasca di Magliano, M. (2012) · Journal of Clinical Investigation · doi:10.1172/jci59227 · Cited by 770
Self-citationOncogenic Kras-induced GM-CSF production promotes the development of pancreatic neoplasia
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Cited by
Macrophages and metabolism in the tumor microenvironment
Vitale, I., Manic, G., Coussens, L. M., Kroemer, G., & Galluzzi, L. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.06.001 · Cited by 1,837
Juneja, V. R., McGuire, K. A., Manguso, R. T., LaFleur, M. W., Collins, N., Haining, W. N., Freeman, G. J., & Sharpe, A. H. (2017) · Journal of Experimental Medicine · doi:10.1084/jem.20160801 · Cited by 851
Role of oncogenic KRAS in the diagnosis, prognosis and treatment of pancreatic cancer
Buscail, L., Bournet, B., & Cordelier, P. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-019-0245-4 · Cited by 721
Regulation of PD-L1 expression in the tumor microenvironment
Yi, M., Niu, M., Xu, L., Luo, S., & Wu, K. (2021) · Journal of Hematology & Oncology · doi:10.1186/s13045-020-01027-5 · Cited by 681
Sullivan, M. R., Danai, L. V., Lewis, C. A., Chan, S. H., Gui, D. Y., Kunchok, T., Dennstedt, E. A., Vander Heiden, M. G., & Muir, A. (2019) · eLife · doi:10.7554/elife.44235 · Cited by 588
Metadata
- Authors
- Zhang, Y., Velez-Delgado, A., Mathew, E., Li, D., Mendez, F. M., Flannagan, K., Rhim, A. D., Simeone, D. M., Beatty, G. L., & Pasca di Magliano, M.
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2016-07-08
- Volume
- 66
- Issue
- 1
- Pages
- 124-136
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- OpenAlex
- W2461513545
- Cited by
- 337
- References
- 17
- FWCI
- 11.27
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Zhang, Y., Velez-Delgado, A., Mathew, E., Li, D., Mendez, F. M., Flannagan, K., Rhim, A. D., Simeone, D. M., Beatty, G. L., & Pasca di Magliano, M. (2017). Myeloid cells are required for PD-1/PD-L1 checkpoint activation and the establishment of an immunosuppressive environment in pancreatic cancer. Gut. https://doi.org/10.1136/gutjnl-2016-312078
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