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Br J Cancer. 2013 Apr 30;108(8):1560-5. doi: 10.1038/bjc.2013.117. Epub 2013 Mar 19.

Exploiting CTLA-4, PD-1 and PD-L1 to reactivate the host immune response against cancer.

Author information

1
Cancer Immunology Unit, Department of Haematology, UCL Cancer Institute, Paul O'Gorman Building, 72 Huntley Street, London WC1E 6BT, UK.

Abstract

The past few years have witnessed something of a renaissance in the field of cancer immunotherapy, relating largely to the clinical advances that have been associated with the development of monoclonal antibodies targeting the immune inhibitory co-receptors CTLA-4 and PD-1 and to the pursuit of genetically modified antigen-redirected adoptive T-cell therapies. These advances are based on a more substantial understanding of the factors restricting effective immune therapies that has been derived from the study of pre-clinical models of tumour growth in immune competent mice. Just as the recognition of the importance of positive co-stimulatory signaling has been instrumental to recent advances in the development of genetically modified antigen-specific adoptive cellular therapies, an increasing awareness of the ability of tumours to subvert multiple immune inhibitory pathways, effectively blunting the development or expansion of any anti-tumour immunity, is fostering the development of novel therapies that appear active as monotherapies but may achieve their greatest impact in combinatorial regimens. This mini-review will focus on attempts to target co-inhibitory members of the immunoglobulin superfamily.

PMID:
23511566
PMCID:
PMC3668483
DOI:
10.1038/bjc.2013.117
[Indexed for MEDLINE]
Free PMC Article

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