The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Costimulatory and coinhibitory receptors in anti‐tumor immunity
Open accessAbstract
Summary: Despite the expression of antigens by tumor cells, spontaneous immune‐mediated rejection of cancer seems to be a rare event. T‐cell receptor engagement by peptide/major histocompatibility complexes constitutes the main signal for the activation of naive T cells but is not sufficient to initiate a productive generation and maintenance of effector cells. Full activation of T cells requires additional signals driven by costimulatory molecules present on activated antigen‐presenting cells but rarely on tumors. Following the discovery of B7‐1 (CD80), several other costimulatory molecules have been shown to contribute to T‐cell activation and have relevance for improving anti‐tumor immunity. Moreover, increasing the understanding of coinhibitory receptors has highlighted key additional pathways that can dominantly inhibit anti‐tumor T‐cell function. Improving positive costimulation, and interfering with negative regulation, continues to represent an attractive immunotherapeutic approach for the treatment of cancer. This review focuses upon those pathways with the highest potential for clinical application in human cancer patients.
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Cites
Control of Regulatory T Cell Development by the Transcription Factor Foxp3
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Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion
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PD-L2 is a second ligand for PD-1 and inhibits T cell activation
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T-cell help for cytotoxic T lymphocytes is mediated by CD40–CD40L interactions
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“In contrast to the costimulatory signal provided by binding of CD28 to B7-1 and B7-2, several lines of evidence pointed to a negative regulatory effect of CTLA-4 on T-cell function, both in vitro and in vivo (128, 129, 132).”
BackgroundCTLA-4 is a second receptor for the B cell activation antigen B7.
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“to B7-1 and B7-2 with an approximately 10- to 20-fold higher affinity than CD28 (16, 130).”
Background
Cited by
The PD‐1 pathway in tolerance and autoimmunity
Francisco, L. M., Sage, P. T., & Sharpe, A. H. (2010) · Immunological Reviews · doi:10.1111/j.1600-065x.2010.00923.x · Cited by 2,300
Immune evasion in cancer: mechanistic basis and therapeutic strategies
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
Woo, S.-R., Turnis, M. E., Goldberg, M. V., Bankoti, J., Selby, M., Nirschl, C. J., Bettini, M. L., Gravano, D. M., Vogel, P., Liu, C. L., et al. (2012) · Cancer Research · doi:10.1158/0008-5472.can-11-1620 · Cited by 1,647
Anti-tumour immunity controlled through mRNA m6A methylation and YTHDF1 in dendritic cells
Han, D., Liu, J., Chen, C., Dong, L., Liu, Y., Chang, R., Huang, X., Liu, Y., Wang, J., Dougherty, U., et al. (2019) · Nature · doi:10.1038/s41586-019-0916-x · Cited by 955
Vaccines for established cancer: overcoming the challenges posed by immune evasion
van der Burg, S. H., Arens, R., Ossendorp, F., van Hall, T., & Melief, C. J. M. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.16 · Cited by 709
Metadata
- Authors
- Driessens, G., Kline, J., & Gajewski, T. F.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2009-04-21
- Volume
- 229
- Issue
- 1
- Pages
- 126-144
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2008428974
- Cited by
- 286
- References
- 28
- FWCI
- 0.65
- Type
- journal article
- Language
- en
- Open access
- green
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