The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Suppressing T cell motility induced by anti–CTLA-4 monotherapy improves antitumor effects
Open accessAbstract
A promising strategy for cancer immunotherapy is to disrupt key pathways regulating immune tolerance, such as cytotoxic T lymphocyte-associated protein 4 (CTLA-4). However, the determinants of response to anti-CTLA-4 mAb treatment remain incompletely understood. In murine models, anti-CTLA-4 mAbs alone fail to induce effective immune responses to poorly immunogenic tumors but are successful when combined with additional interventions, including local ionizing radiation (IR) therapy. We employed an established model based on control of a mouse carcinoma cell line to study endogenous tumor-infiltrating CD8+ T lymphocytes (TILs) following treatment with the anti-CTLA-4 mAb 9H10. Alone, 9H10 monotherapy reversed the arrest of TILs with carcinoma cells in vivo. In contrast, the combination of 9H10 and IR restored MHC class I-dependent arrest. After implantation, the carcinoma cells had reduced expression of retinoic acid early inducible-1 (RAE-1), a ligand for natural killer cell group 2D (NKG2D) receptor. We found that RAE-1 expression was induced by IR in vivo and that anti-NKG2D mAb blocked the TIL arrest induced by IR/9H10 combination therapy. These results demonstrate that anti-CTLA-4 mAb therapy induces motility of TIL and that NKG2D ligation offsets this effect to enhance TILs arrest and antitumor activity.
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Apetoh, L., Ghiringhelli, F., Tesniere, A., Obeid, M., Ortiz, C., Criollo, A., Mignot, G., Maiuri, M. C., Ullrich, E., Saulnier, P., et al. (2007) · Nature Medicine · doi:10.1038/nm1622 · Cited by 3,056 · cited 1×
“Reduction of metastases may arise from increased priming of naive tumor-specific T cells by the in situ vaccination generated by IR (29, 31), as well as the improvement of tumor-specific CD8+ memory T cells by anti–CTLA-4 (20).”
Rosenberg, S. A., Packard, B. S., Aebersold, P. M., Solomon, D., Topalian, S. L., Toy, S. T., Simon, P., Lotze, M. T., Yang, J. C., Seipp, C. A., et al. (1988) · New England Journal of Medicine · doi:10.1056/nejm198812223192527 · Cited by 2,389
Trans-endocytosis of CD80 and CD86: a molecular basis for the cell-extrinsic function of CTLA-4
Qureshi, O. S., Zheng, Y., Nakamura, K., Attridge, K., Manzotti, C., Schmidt, E. M., Baker, J., Jeffery, L. E., Kaur, S., Briggs, Z., et al. (2011) · Science · doi:10.1126/science.1202947 · Cited by 1,860 · cited 1×
“Non-autonomous effects of CTLA-4 include the reduction of CD80 and CD86 from the surface of dentritic cells by regulatory and effector T cell–mediated trogocytosis (11, 12).”
Dewan, M. Z., Galloway, A. E., Kawashima, N., Dewyngaert, J. K., Babb, J. S., Formenti, S. C., & Demaria, S. (2009) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-09-0265 · Cited by 1,678
Self-citationThe DNA damage pathway regulates innate immune system ligands of the NKG2D receptor
Gasser, S., Orsulic, S., Brown, E. J., & Raulet, D. H. (2005) · Nature · doi:10.1038/nature03884 · Cited by 1,308
Rae1 and H60 ligands of the NKG2D receptor stimulate tumour immunity
Diefenbach, A., Jensen, E. R., Jamieson, A. M., & Raulet, D. H. (2001) · Nature · doi:10.1038/35093109 · Cited by 1,083
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Lugade, A. A., Moran, J. P., Gerber, S. A., Rose, R. C., Frelinger, J. G., & Lord, E. M. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.174.12.7516 · Cited by 966
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Quezada, S. A. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27745 · Cited by 700 · cited 1×
“Consistent with previous data indicating that anti–CTLA-4 mAb in combination with vaccination, but not as monotherapy, results in increased intratumoral T cell infiltration (44), only the combination of IR and 9H10 resulted in a significant increase (P < 0.”
Cited by
Radiotherapy and immunotherapy: a beneficial liaison?
Weichselbaum, R. R., Liang, H., Deng, L., & Fu, Y.-X. (2017) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2016.211 · Cited by 1,070
Radiotherapy induces responses of lung cancer to CTLA-4 blockade
Formenti, S. C., Rudqvist, N.-P., Golden, E., Cooper, B., Wennerberg, E., Lhuillier, C., Vanpouille-Box, C., Friedman, K., Ferrari de Andrade, L., Wucherpfennig, K. W., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0232-2 · Cited by 928
Self-citationGolden, E. B., Demaria, S., Schiff, P. B., Chachoua, A., & Formenti, S. C. (2013) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-13-0115 · Cited by 688
Self-citationGolden, E. B., Chhabra, A., Chachoua, A., Adams, S., Donach, M., Fenton-Kerimian, M., Friedman, K., Ponzo, F., Babb, J. S., Goldberg, J., et al. (2015) · The Lancet Oncology · doi:10.1016/s1470-2045(15)00054-6 · Cited by 667
Self-citationCancer immunotherapy: Opportunities and challenges in the rapidly evolving clinical landscape
Emens, L. A., Ascierto, P. A., Darcy, P. K., Demaria, S., Eggermont, A. M. M., Redmond, W. L., Seliger, B., & Marincola, F. M. (2017) · European Journal of Cancer · doi:10.1016/j.ejca.2017.01.035 · Cited by 566
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Metadata
- Authors
- Ruocco, M. G., Pilones, K. A., Kawashima, N., Cammer, M., Huang, J., Babb, J. S., Liu, M., Formenti, S. C., Dustin, M. L., & Demaria, S.
- Venue
- Journal of Clinical Investigation
- Published
- 2012-10-01
- Volume
- 122
- Issue
- 10
- Pages
- 3718-3730
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2046834643
- Cited by
- 187
- References
- 12
- FWCI
- 8.52
- Type
- journal article
- Language
- en
- Open access
- green
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- Ruocco, M. G., Pilones, K. A., Kawashima, N., Cammer, M., Huang, J., Babb, J. S., Liu, M., Formenti, S. C., Dustin, M. L., & Demaria, S. (2012). Suppressing T cell motility induced by anti–CTLA-4 monotherapy improves antitumor effects. Journal of Clinical Investigation. https://doi.org/10.1172/jci61931
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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