4.6 Review

Role of cancer-associated fibroblast subpopulations in immune infiltration, as a new means of treatment in cancer

期刊

IMMUNOLOGICAL REVIEWS
卷 302, 期 1, 页码 259-272

出版社

WILEY
DOI: 10.1111/imr.12978

关键词

cancer; cancer‐ associated fibroblasts; heterogeneity; immunosuppression; immunotherapy; T lymphocytes

资金

  1. SIRIC [INCa-DGOS-4654]
  2. Ligue Nationale Contre le Cancer
  3. Association pour la Recherche sur le Cancer
  4. ICGex [ANR-10-EQPX-03]
  5. Institut Curie [PIC3i CAFi, PIC TME/T-MEGA]
  6. Association Ruban Rose
  7. Institut National Du Cancer [CaLYS INCa-11692, INCa-DGOS-Inserm-12554, STROMAE INCa-DGOS-9963]
  8. Institut National de la Sante et de la Recherche Medicale [PC201317]
  9. Fondation Simone et Cino Del Duca
  10. Fondation Chercher et Trouver

向作者/读者索取更多资源

CAF in the tumor microenvironment play crucial roles in promoting tumor growth, modulating immune cell activity, and creating an immunosuppressive microenvironment. Understanding the heterogeneity and functions of CAF is vital for exploring their interactions with immune cells, driving cancer progression, and developing therapeutic strategies targeting CAF subpopulations.
The tumor microenvironment (TME) has been identified as one of the driving factors of tumor progression and invasion. Within this microenvironment, cancer-associated fibroblasts (CAF) have multiple tumor-promoting functions and play key roles in drug resistance, through multiple mechanisms, including extracellular matrix (ECM) remodeling, production of growth factors, cytokines, and chemokines, and modulation of metabolism and angiogenesis. More recently, a growing body of evidence has shown that CAF also modulate immune cell activity and suppress anti-tumor immune response. In this review, we describe the current knowledge on CAF heterogeneity in terms of identity and functions. Moreover, we analyze how distinct CAF subpopulations differentially interact with immune cells, with a particular focus on T lymphocytes. We address how specific CAF subsets contribute to cancer progression through induction of an immunosuppressive microenvironment. Finally, we highlight potential therapeutic strategies for targeting CAF subpopulations in cancer.

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