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Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles
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CD73-Mediated Immunosuppression Is Linked to a Specific Fibroblast Population That Paves the Way for New Therapy in

Ilaria Magagna1,2,3, Nicolas Gourdin3, Yann Kieffer1,2

  • 1Equipe labellisée Ligue Nationale Contre le Cancer, Stress and Cancer Laboratory, Institut Curie, PSL Research University, 26, rue d'Ulm, 75005 Paris, France.

Cancers
|December 10, 2021
PubMed
Abstract

Insights

Cancer-associated fibroblasts (CAF), specifically CAF-S1, promote breast cancer immunosuppression via CD73. Targeting CD73 may enhance immunotherapy by reducing regulatory T lymphocytes (Tregs) and immune checkpoint expression.

Area of Science:

  • Oncology
  • Immunology
  • Cancer Biology

Background:

  • Cancer-associated fibroblasts (CAF) are a heterogeneous cell population with diverse roles in breast cancer.
  • A specific CAF subpopulation, CAF-S1, has been identified as a promoter of immunosuppression and resistance to immunotherapy.

Purpose of the Study:

  • To investigate the role of CD73/NT5E in CAF-S1-mediated immunosuppression within the breast cancer microenvironment.
  • To explore the potential of targeting CD73 for enhancing anti-tumor immunity.

Main Methods:

  • Analysis of human breast cancer samples to assess CD73 protein levels in CAF-S1.
  • Correlation analysis between CD73 expression and regulatory T lymphocyte (Treg) infiltration.
  • Functional assays using primary CAF-S1 and blocking anti-CD73 antibodies in relevant systems.

Main Results:

  • CD73 protein specifically accumulates in CAF-S1 within breast cancer stroma.
  • CD73 expression in CAF-S1 correlates with increased Treg infiltration.
  • CAF-S1 promotes the accumulation of PD-1+ and CTLA-4+ Tregs.
  • Blocking CD73 on CAF-S1 reduces immunosuppression and prevents immune checkpoint expression on Tregs.

Conclusions:

  • CD73 plays a critical role in CAF-S1-mediated immunosuppression in breast cancer.
  • Targeting CD73, in combination with immune-checkpoint inhibitors, shows potential for clinical benefit in breast cancer patients.
  • This therapeutic strategy may enhance anti-tumor immune responses by overcoming CAF-S1-driven immunosuppression.
Keywords:
CAF subsetsTregsanti-CD73 antibodybreast cancerimmunosuppression

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