The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
CD73-Deficient Mice Have Increased Antitumor Immunity and Are Resistant to Experimental Metastasis
Abstract
CD73 is a cell-surface enzyme that suppresses immune responses by producing extracellular adenosine. In this study, we employed CD73 gene-targeted mice to investigate the role of host-derived CD73 on antitumor immunity and tumor cell metastasis. We found that CD73 ablation significantly suppressed the growth of ovalbumin-expressing MC38 colon cancer, EG7 lymphoma, AT-3 mammary tumors, and B16F10 melanoma. The protective effect of CD73 deficiency on primary tumors was dependent on CD8+ T cells and associated with an increased frequency of antigen-specific CD8+ T cells in peripheral blood and tumors and increased antigen-specific IFN-γ production. Replicate studies in bone marrow chimeras established that both hematopoietic and nonhematopoietic expression of CD73 was important to promote tumor immune escape. Using adoptive reconstitution of T regulatory cell (Treg)–depleted DEREG (depletion of regulatory T cells) mice, we demonstrated that part of the protumorigenic effect of Tregs was dependent on their expression of CD73. CD73-deficient mice were also protected against pulmonary metastasis of B16F10 melanoma cells after intravenous injection. Unexpectedly, we found that the prometastatic effect of host-derived CD73 was dependent on CD73 expression on nonhematopoietic cells. CD73 expression on nonhematopoietic cells, most likely endothelial cells, was critical for promoting lung metastasis in a manner independent from immunosuppressive effects. Notably, in vivo blockade of CD73 with a selective inhibitor or anti-CD73 monoclonal antibody significantly reduced tumor growth and metastasis of CD73-negative tumors. Taken together, our findings indicate that CD73 may be targeted at multiple levels to induce anticancer effects including at the level of tumor cells, Tregs, and nonhematopoietic cells. Cancer Res; 71(8); 2892–900. ©2011 AACR.
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Ohta, A., & Sitkovsky, M. (2001) · Nature · doi:10.1038/414916a · Cited by 1,334
A2A adenosine receptor protects tumors from antitumor T cells
Ohta, A., Gorelik, E., Prasad, S. J., Ronchese, F., Lukashev, D., Wong, M. K. K., Huang, X., Caldwell, S., Liu, K., Smith, P., et al. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605251103 · Cited by 1,065
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Synnestvedt, K., Furuta, G. T., Comerford, K. M., Louis, N. A., Karhausen, J., Eltzschig, H. K., Hansen, K. R., Thompson, L. F., & Colgan, S. P. (2002) · Journal of Clinical Investigation · doi:10.1172/jci15337 · Cited by 679
Synnestvedt, K., Furuta, G. T., Comerford, K. M., Louis, N., Karhausen, J., Eltzschig, H. K., Hansen, K. R., Thompson, L. F., & Colgan, S. P. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0215337 · Cited by 660
Cyclic adenosine monophosphate is a key component of regulatory T cell–mediated suppression
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Anti-CD73 antibody therapy inhibits breast tumor growth and metastasis
Stagg, J., Divisekera, U., McLaughlin, N., Sharkey, J., Pommey, S., Denoyer, D., Dwyer, K. M., & Smyth, M. J. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0908801107 · Cited by 572
Self-citationExtracellular adenosine triphosphate and adenosine in cancer
Stagg, J., & Smyth, M. J. (2010) · Oncogene · doi:10.1038/onc.2010.292 · Cited by 571
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Vinay, D. S., Ryan, E. P., Pawelec, G., Talib, W. H., Stagg, J., Elkord, E., Lichtor, T., Decker, W. K., Whelan, R. L., Kumara, H. M. C. S., et al. (2015) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2015.03.004 · Cited by 1,625
Self-citationThe ectonucleotidases CD 39 and CD 73: Novel checkpoint inhibitor targets
Allard, B., Longhi, M. S., Robson, S. C., & Stagg, J. (2017) · Immunological Reviews · doi:10.1111/imr.12528 · Cited by 927
Self-citationZitvogel, L., Galluzzi, L., Smyth, M. J., & Kroemer, G. (2013) · Immunity · doi:10.1016/j.immuni.2013.06.014 · Cited by 870
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Metadata
- Authors
- Stagg, J., Divisekera, U., Duret, H., Sparwasser, T., Teng, M. W. L., Darcy, P. K., & Smyth, M. J.
- Venue
- Cancer Research
- Published
- 2011-04-13
- Volume
- 71
- Issue
- 8
- Pages
- 2892-2900
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2168786562
- Cited by
- 401
- References
- 35
- FWCI
- 18.44
- Type
- journal article
- Language
- en
- Open access
- closed
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- Stagg, J., Divisekera, U., Duret, H., Sparwasser, T., Teng, M. W. L., Darcy, P. K., & Smyth, M. J. (2011). CD73-Deficient Mice Have Increased Antitumor Immunity and Are Resistant to Experimental Metastasis. Cancer Research. https://doi.org/10.1158/0008-5472.can-10-4246
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