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Molecular pathways: targeting CD96 and TIGIT for cancer immunotherapy

Blake, S. J., Dougall, W. C., Miles, John James, Teng, M. W. L. and Smyth, M. J. 2016. Molecular pathways: targeting CD96 and TIGIT for cancer immunotherapy. Clinical Cancer Research 22 (21) , pp. 5183-5188. 10.1158/1078-0432.CCR-16-0933

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Abstract

The receptors CD96 and TIGIT are expressed on the surface of T and natural killer (NK) cells, and recent studies suggest both play important inhibitory roles in immune function. CD96 has been shown to modulate immune cell activity in mice, with Cd96−/− mice displaying hypersensitive NK-cell responses to immune challenge and significant tumor resistance. TIGIT overexpression has been shown to reduce NK-cell–mediated cytotoxicity. TIGIT is also upregulated on T cells during cancer and chronic viral infection, with expression associated with effector T-cell exhaustion and increased regulatory T-cell suppression. The counterbalance between the putative inhibitory CD96 and TIGIT receptors and the activating receptor, CD226, offers unique strategies for immuno-oncology drug development. Blocking CD96 or TIGIT with mAbs has been shown to improve tumor control in mice, in particular when used in combination with PD-1/PD-L1 blockade. These results have highlighted these pathways as promising new targets for immune modulation. This review will examine the rationale behind targeting CD96 and TIGIT, and discuss the potential approaches in translating these preclinical findings into novel clinical agents.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Publisher: American Association for Cancer Research
ISSN: 1078-0432
Date of First Compliant Deposit: 16 July 2018
Last Modified: 17 Jul 2018 04:32
URI: http://orca.cf.ac.uk/id/eprint/105596

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