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Published on: May 2, 2025
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TIGIT-CD226-PVR axis: advancing immune checkpoint blockade for cancer immunotherapy
Eugene Y Chiang1, Ira Mellman2
1Cancer Immunology, Genentech Inc, South San Francisco, California, USA.
Journal for Immunotherapy of Cancer
|April 5, 2022
Summary
Immune checkpoint TIGIT (T cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory domains) regulates T cell activity. Targeting TIGIT offers a promising new avenue for cancer immunotherapy by enhancing antitumor immune responses.
Area of Science:
- Immunology
- Oncology
- Cancer Immunotherapy
Background:
- Cancer immune evasion is a major challenge in oncology.
- Approved immunotherapies like CTLA-4 and PD-1/PD-L1 blockade enhance T cell function.
- New immune checkpoint targets are needed to improve cancer treatment.
Purpose of the Study:
- To review the role of TIGIT as an immune checkpoint inhibitor.
- To discuss the interplay between TIGIT and its counter-receptor CD226.
- To highlight TIGIT's potential as a next-generation cancer immunotherapy.
Main Methods:
- Review of current scientific literature on TIGIT and cancer immunology.
- Analysis of TIGIT's mechanism of action and its interaction with CD226.
- Summary of clinical development status for TIGIT-directed therapies.
Main Results:
- TIGIT is an inhibitory immune checkpoint receptor.
- TIGIT negatively regulates the costimulatory receptor CD226, impacting T cell activity.
- Numerous TIGIT-blocking antibodies are in clinical trials, showing therapeutic promise.
Conclusions:
- TIGIT represents a significant immune checkpoint axis in cancer.
- Modulating the TIGIT/CD226 pathway holds potential for enhancing antitumor immunity.
- TIGIT-targeted therapies are poised to be a key advancement in cancer immunotherapy.
Keywords:
Costimulatory and Inhibitory T-Cell ReceptorsImmunotherapyLymphocytes, Tumor-InfiltratingReviewMore Related Videos
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