The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
TIGIT in cancer immunotherapy
Open accessAbstract
Tumors evade immune-mediated recognition through multiple mechanisms of immune escape. On chronic tumor antigen exposure, T cells become dysfunctional/exhausted and upregulate various checkpoint inhibitory receptors (IRs) that limit T cells’ survival and function. During the last decade, immunotherapies targeting IRs such as programmed cell death receptor 1 (PD-1) and anticytotoxic T lymphocyte-associated antigen 4 (CTLA-4) have provided ample evidence of clinical benefits in many solid tumors. Beyond CTLA-4 and PD-1, multiple other IRs are also targeted with immune checkpoint blockade in the clinic. Specifically, T cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT) is a promising new target for cancer immunotherapy. TIGIT is upregulated by immune cells, including activated T cells, natural killer cells, and regulatory T cells. TIGIT binds to two ligands, CD155 (PVR) and CD112 (PVRL2, nectin-2), that are expressed by tumor cells and antigen-presenting cells in the tumor microenvironment. There is now ample evidence that the TIGIT pathway regulates T cell-mediated and natural killer cell-mediated tumor recognition in vivo and in vitro. Dual PD-1/TIGIT blockade potently increases tumor antigen-specific CD8+ T cell expansion and function in vitro and promotes tumor rejection in mouse tumor models. These findings support development of ongoing clinical trials with dual PD-1/TIGIT blockade in patients with cancer.
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Cites
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Cited by
Antigen presentation in cancer: insights into tumour immunogenicity and immune evasion
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Immune checkpoint therapy—current perspectives and future directions
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Targeting LAG-3, TIM-3, and TIGIT for cancer immunotherapy
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Metadata
- Authors
- Chauvin, J.-M., & Zarour, H. M.
- Venue
- Journal for ImmunoTherapy of Cancer
- Publisher
- BMJ
- Published
- 2020-09
- Volume
- 8
- Issue
- 2
- Pages
- e000957
- ISSN
- 2051-1426 (ISSN-L)
- OpenAlex
- W3084404519
- Cited by
- 794
- References
- 8
- FWCI
- 31.28
- Type
- journal article
- Language
- en
- Open access
- gold
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