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Updated: Mar 20, 2026

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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
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Regulation of the immune CD155-CD226-TIGIT axis by cyclin D-CDK4/6
Anne Fassl1,2,3,4,5, Miriam Palacios Espinoza1,2, Deborah Butter1,2
1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215.
Summary
CDK4/6 inhibitors upregulate CD155 and downregulate TIGIT, enhancing anti-tumor immunity. Combining CDK4/6 inhibitors with anti-TIGIT antibodies may offer synergistic effects against breast cancer.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Cyclin-dependent kinase 4/6 (CDK4/6) regulates cell proliferation and is a target for breast cancer therapy.
- CDK4/6 inhibitors halt cell-cycle progression but may also influence anti-tumor immunity.
Purpose of the Study:
- To investigate the impact of CDK4/6 inhibition on the CD155-CD226-TIGIT pathway.
- To explore the potential of modulating this pathway to enhance anti-tumor immune responses.
Main Methods:
- Analysis of CD155 and TIGIT expression in human breast cancer cell lines and patient samples.
- In vivo studies using mouse mammary carcinoma allograft models.
- Evaluation of paired pre-/on-treatment biopsies from patients receiving CDK4/6 inhibitor monotherapy.
Main Results:
- CDK4/6 inhibition increased surface CD155 protein expression on cancer cells.
- CDK4/6 inhibition decreased the immuno-inhibitory receptor TIGIT on tumor-infiltrating lymphocytes.
- Observed effects in cell lines, mouse models, and human breast tumors.
Conclusions:
- CDK4/6 inhibition may shift the balance towards immunostimulatory CD155-CD226 interactions over immunoinhibitory CD155-TIGIT interactions.
- This mechanism could augment anti-tumor immunity.
- Coadministration of CDK4/6 inhibitors and anti-TIGIT antibodies may synergistically enhance anti-tumor effects.
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