Language

English

Publication Date

7-8-2024

Journal

Cancer Cell

DOI

10.1016/j.ccell.2024.05.025

PMID

38906155

PMCID

PMC11413804

PubMedCentral® Posted Date

7-8-2025

PubMedCentral® Full Text Version

Author MSS

Abstract

Tumor-specific CD8+ T cells are frequently dysfunctional and unable to halt tumor growth. We investigated whether tumor-specific CD4+ T cells can be enlisted to overcome CD8+ T cell dysfunction within tumors. We find that the spatial positioning and interactions of CD8+ and CD4+ T cells, but not their numbers, dictate anti-tumor responses in the context of adoptive T cell therapy as well as immune checkpoint blockade (ICB): CD4+ T cells must engage with CD8+ T cells on the same dendritic cell during the effector phase, forming a three-cell-type cluster (triad) to license CD8+ T cell cytotoxicity and cancer cell elimination. When intratumoral triad formation is disrupted, tumors progress despite equal numbers of tumor-specific CD8+ and CD4+ T cells. In patients with pleural mesothelioma treated with ICB, triads are associated with clinical responses. Thus, CD4+ T cells and triads are required for CD8+ T cell cytotoxicity during the effector phase and tumor elimination.

Keywords

Humans, CD8-Positive T-Lymphocytes, Animals, CD4-Positive T-Lymphocytes, Mice, Immunotherapy, Neoplasms, Immune Checkpoint Inhibitors, Mice, Inbred C57BL, Immunotherapy, Adoptive, Dendritic Cells, Cell Line, Tumor, Tumor Microenvironment

Published Open-Access

yes

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