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Updated: Sep 19, 2025

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice

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Published on: June 12, 2021

Sustained Macrophage Reprogramming Is Required for CD8+ T cell-Dependent Long-Term Tumor Eradication.

Carolina Jardim^1,2, Marta Bica^1,2, Mariana Reis-Sobreiro¹

¹Gulbenkian Institute for Molecular Medicine, Lisbon, Portugal.

Cancer Immunology Research

|June 5, 2025

Summary

This summary is machine-generated.

Myeloid cell treatment (MCT) with TLR3 and CD40 agonists reprograms tumor-associated macrophages (TAMs) to fight breast cancer. Repeated MCT sustains this antitumor effect, activating CD8+ T cells for long-term tumor eradication.

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Transduction and Expansion of Primary T Cells in Nine Days with Maintenance of Central Memory Phenotype

Transduction and Expansion of Primary T Cells in Nine Days with Maintenance of Central Memory Phenotype

Published on: March 18, 2020

Area of Science:

Immunology
Oncology
Cancer Research

Background:

Tumor-associated macrophages (TAMs) have a complex role in cancer, influencing both tumor progression and immune responses.
Understanding the specific functional states and molecular drivers of antitumor TAMs is crucial but challenging.

Purpose of the Study:

To investigate the potential of a combined TLR3 and CD40 agonist treatment (myeloid cell treatment, MCT) to reprogram TAMs into an antitumor phenotype.
To elucidate the temporal dynamics and molecular mechanisms underlying TAM reprogramming and its impact on tumor regression.

Main Methods:

Intratumoral administration of TLR3 and CD40 agonists in an orthotopic mouse breast cancer model.
Single-cell RNA sequencing of TAMs at various time points post-treatment.
Analysis of immune cell activation, particularly CD8+ T cells, and tumor eradication.

Main Results:

MCT induced a transient antitumor TAM phenotype characterized by specific markers (e.g., iNOS, CD38) peaking at 12 hours.
This phenotype shifted by 72 hours to TAMs with mixed tumor-promoting and limiting features.
Repeated MCT administration was necessary to maintain the antitumor TAM state, leading to CD8+ T cell activation and tumor eradication.
Reactive oxygen species and TNF-α were identified as key mediators of TAM-driven tumor control.

Conclusions:

The antitumor reprogramming of TAMs by MCT is transient, highlighting a vulnerability in this therapeutic approach.
Sustained antitumor immunity and tumor eradication can be achieved through repeated administrations of MCT, overcoming the transient nature of TAM reprogramming.
This study provides insights into manipulating TAMs for effective cancer immunotherapy.