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A Real-time Potency Assay for Chimeric Antigen Receptor T Cells Targeting Solid and Hematological Cancer Cells
Published on: November 12, 2019
TIGIT and CD96: new checkpoint receptor targets for cancer immunotherapy
William C Dougall1, Sema Kurtulus2, Mark J Smyth1,3
1QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Abstract:
While therapies targeting the co-inhibitory or immune checkpoint receptors PD-1 and CTLA-4 have shown remarkable success in many cancers, not all patients benefit from these therapies. This has catalyzed enormous interest in the targeting of other immune checkpoint receptors. In this regard, TIGIT and CD96 have recently entered the limelight as novel immune checkpoint receptor targets. TIGIT and CD96 together with the co-stimulatory receptor CD226 form a pathway that is analogous to the CD28/CTLA-4 pathway, in which shared ligands and differential receptor:ligand affinities fine-tune the immune response. Although the roles of TIGIT and CD96 as immune checkpoint receptors in T cell and natural killer cell biology are just beginning to be uncovered, accumulating data support the targeting of these receptors for improving anti-tumor immune responses. A clear understanding of the immune cell populations regulated by TIGIT and CD96 is key to the design of immunotherapies that target these receptors in combination with other existing immune checkpoint blockade therapies.
Insights
New immune checkpoint targets, TIGIT and CD96, offer potential for improving cancer immunotherapies. Understanding their roles in T cells and NK cells is crucial for developing effective combination treatments.
Area of Science:
- Immunology
- Cancer Biology
- Drug Discovery
Background:
- Immune checkpoint inhibitors targeting PD-1 and CTLA-4 have advanced cancer therapy but lack universal efficacy.
- This necessitates exploration of alternative immune checkpoint receptors for enhanced anti-tumor immunity.
Purpose of the Study:
- To highlight TIGIT and CD96 as promising novel immune checkpoint targets.
- To emphasize the importance of understanding the TIGIT/CD96/CD226 pathway in immune regulation.
- To underscore the potential of targeting these receptors for improved cancer immunotherapy.
Main Methods:
- Review of current literature on TIGIT, CD96, and CD226.
- Analysis of the analogous CD28/CTLA-4 pathway.
- Exploration of immune cell populations regulated by TIGIT and CD96.
Main Results:
- TIGIT and CD96 function as immune checkpoint receptors, analogous to CTLA-4.
- Shared ligands and differential affinities fine-tune immune responses within this pathway.
- Emerging data support TIGIT and CD96 targeting for boosting anti-tumor immunity.
Conclusions:
- TIGIT and CD96 are emerging as critical targets in cancer immunotherapy.
- Understanding the immune cell populations modulated by TIGIT and CD96 is essential.
- Targeting TIGIT and CD96 in combination with existing therapies may improve patient outcomes.
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