The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Tumor Evasion from T Cell Surveillance
Open accessAbstract
An intact immune system is essential to prevent the development and progression of neoplastic cells in a process termed immune surveillance. During this process the innate and the adaptive immune systems closely cooperate and especially T cells play an important role to detect and eliminate tumor cells. Due to the mechanism of central tolerance the frequency of T cells displaying appropriate arranged tumor‐peptide‐specific‐T‐cell receptors is very low and their activation by professional antigen‐presenting cells, such as dendritic cells, is frequently hampered by insufficient costimulation resulting in peripheral tolerance. In addition, inhibitory immune circuits can impair an efficient antitumoral response of reactive T cells. It also has been demonstrated that large tumor burden can promote a state of immunosuppression that in turn can facilitate neoplastic progression. Moreover, tumor cells, which mostly are genetically instable, can gain rescue mechanisms which further impair immune surveillance by T cells. Herein, we summarize the data on how tumor cells evade T‐cell immune surveillance with the focus on solid tumors and describe approaches to improve anticancer capacity of T cells.
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Cites
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Metadata
- Authors
- Töpfer, K., Kempe, S., Müller, N., Schmitz, M., Bachmann, M., Cartellieri, M., Schackert, G., & Temme, A.
- Venue
- BioMed Research International
- Publisher
- Wiley
- Published
- 2011-01
- Volume
- 2011
- Issue
- 1
- Pages
- 918471-918471
- ISSN
- 1110-7243 (ISSN-L)
- 2314-6133
- 2314-6141
- OpenAlex
- W2165957370
- Cited by
- 171
- References
- 17
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Töpfer, K., Kempe, S., Müller, N., Schmitz, M., Bachmann, M., Cartellieri, M., Schackert, G., & Temme, A. (2011). Tumor Evasion from T Cell Surveillance. BioMed Research International. https://doi.org/10.1155/2011/918471
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