The Remarkable Plasticity of Macrophages: A Chance to Fight Cancer

Nadège Bercovici1,2,3, Marion V Guérin1,2,3, Alain Trautmann1,2,3

  • 1INSERM, U1016, Institut Cochin, Paris, France.

Insights

Tumor-associated macrophages (TAM) can hinder anti-tumor immunity or, with immunotherapy, help T cells eradicate cancer. This review explores TAM

Area of Science:

  • Immunology
  • Oncology
  • Cancer Research

Background:

  • Tumor-associated macrophages (TAM) are prevalent in advanced tumors and typically promote cancer growth.
  • TAM can inhibit anti-tumor immune responses by limiting the activity of tumor-infiltrating lymphocytes (TIL).
  • Therapeutic strategies have focused on depleting TAM based on their pro-tumoral functions.

Purpose of the Study:

  • To review the dual role of TAM in their interactions with TIL.
  • To summarize mechanisms by which TAM inhibit T cell activity in growing tumors.
  • To discuss the potential of TAM to cooperate with T cells in tumor eradication following immunotherapy.

Main Methods:

  • Literature review of studies on TAM-TIL interactions.
  • Analysis of mechanisms of TAM-mediated T cell inhibition.
  • Synthesis of findings on TAM reprogramming in combination with T cell-based immunotherapy.

Main Results:

  • TAM exhibit context-dependent functions, acting as either pro-tumoral or anti-tumoral mediators.
  • During tumor regression induced by immunotherapy, TAM can transition to an anti-tumoral phenotype.
  • TAM can cooperate with TIL to achieve tumor eradication after specific stimulation.

Conclusions:

  • TAM possess a dual role in cancer immunity, influencing tumor progression and regression.
  • Understanding TAM plasticity is crucial for developing effective cancer immunotherapies.
  • Combining TAM reprogramming with T cell-based immunotherapy holds promise for enhanced cancer treatment.

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