CD155 and Its Receptors as Targets for Cancer Therapy
Rossella Paolini1, Rosa Molfetta1
1Department of Molecular Medicine, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, 00161 Rome, Italy.
CD155, a tumor-promoting molecule, interacts with immune receptors DNAM-1 and TIGIT. Targeting CD155 or modulating these interactions offers potential cancer immunotherapies.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- CD155 (poliovirus receptor) is overexpressed in tumors, promoting migration and proliferation.
- CD155 acts as a ligand for DNAM-1 (activating) and TIGIT (inhibitory) receptors on lymphocytes.
- TIGIT functions as an immune checkpoint, counteracting DNAM-1's anti-tumor surveillance in advanced cancers.
Purpose of the Study:
- To review therapeutic strategies targeting CD155 and its associated immune pathways.
- To highlight the complex and debated role of CD155 in tumor progression.
Main Methods:
- Literature review of pre-clinical and clinical studies.
- Analysis of CD155's interactions with DNAM-1 and TIGIT.
- Evaluation of therapeutic approaches including direct CD155 targeting and immune checkpoint modulation.
Main Results:
- Pre-clinical studies suggest targeting CD155 or enhancing DNAM-1 function as viable therapies.
- Anti-TIGIT antibodies are in clinical trials, alone or in combination therapies.
- CD155's precise role in tumor progression remains a subject of ongoing research and debate.
Conclusions:
- Targeting the CD155/DNAM-1/TIGIT axis presents promising avenues for cancer immunotherapy.
- Further research is needed to fully elucidate CD155's controversial role and optimize therapeutic strategies.
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