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Updated: Jan 21, 2026

Studying the Role of Alveolar Macrophages in Breast Cancer Metastasis
Published on: June 26, 2016
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.
Abstract:
It is well established that tumor-associated macrophages (TAM) found in most advanced tumors have a pro-tumoral role. In this context, TAM limit the activity of tumor-infiltrating lymphocytes (TIL), and a number of mechanisms have been described including a trapping in the stroma, impeding TIL to reach malignant cells. Based on these results, a number of therapeutic approaches have been designed to deplete TAM. However, during tumor regression induced by immunotherapeutic treatments, recent studies revealed that TAM can switch from pro-tumoral to anti-tumoral and actively cooperate with TIL. Here, we will review the two faces of TAM in their interaction with TIL. We will summarize how they can inhibit T cell activities in growing tumors, and how they may also, together with T cells, successfully contribute to tumor eradication after an appropriate stimulation. Finally, we will discuss current promising therapies combining TAM reprogramming with T cell-based immunotherapy.
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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