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Updated: Jun 7, 2026

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
Published on: March 7, 2025
T cell coinhibition in prostate cancer: new immune evasion pathways and emerging therapeutics
Yael S Barach1, Jun Sik Lee1, Xingxing Zang2
1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Abstract:
T cell-mediated adaptive immune response is controlled by both positive costimulation and negative coinhibition, generated mainly by the interaction between the B7 family and their receptor CD28 family. Coinhibition is exploited by prostate cancer as an immune evasion pathway. Overexpression of coinhibitory B7x and B7-H3 in prostate cancer correlates with poor disease outcome, whereas tumor-infiltrating immune cells have enhanced expression of PD-L1 and its receptor PD-1. New insights into the complex mechanisms governing B7 expression in the tumor microenvironment have been reported and therapies aimed at overcoming T cell coinhibition with antagonistic monoclonal antibodies are emerging as effective tumor immunotherapies. Therapies that block B7x and B7-H3, either as monotherapies or in synergism with traditional therapies, should be pursued.
Insights
Prostate cancer uses coinhibition to evade the immune system. Blocking B7x and B7-H3 offers a promising immunotherapy strategy, potentially enhancing traditional treatments for better outcomes.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Adaptive immunity relies on T cell costimulation and coinhibition.
- The B7 family and CD28 family receptors mediate these interactions.
- Prostate cancer exploits coinhibitory pathways for immune evasion.
Purpose of the Study:
- To investigate the role of coinhibitory molecules in prostate cancer's immune evasion.
- To explore the therapeutic potential of targeting coinhibitory B7x and B7-H3 in prostate cancer.
Main Methods:
- Analysis of B7x, B7-H3, PD-L1, and PD-1 expression in prostate tumors.
- Review of emerging immunotherapies targeting T cell coinhibition.
Main Results:
- Overexpression of coinhibitory B7x and B7-H3 correlates with poor prostate cancer outcomes.
- Tumor-infiltrating immune cells show increased PD-L1 and PD-1 expression.
- Antagonistic monoclonal antibodies targeting coinhibition are effective immunotherapies.
Conclusions:
- Targeting coinhibitory B7x and B7-H3 is a viable therapeutic strategy for prostate cancer.
- Blocking these molecules may synergize with traditional therapies.
- Further research into B7 expression mechanisms in the tumor microenvironment is warranted.
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