CD4 <sup>+</sup> T cells impair tumor growth through IL-3 and TNF-dependent vascular damage

Most cancer immunotherapy strategies are focused on direct tumor killing by immune cells, especially T lymphocytes. Clinical and conceptual limitations of these approaches create a need for additional strategies. We identified a tumor stroma–targeting mechanism in which tumor antigen–specific CD4 + T cells inhibit tumor growth through myeloid cell and tumor necrosis factor (TNF)–dependent vascular damage. Multiplex immunofluorescence and single-cell and tissue transcriptomics showed that CD4 + T cells trigger the formation of perivascular myeloid cell clusters containing “classically activated” macrophages that produce TNF in response to T cell–derived interleukin-3. TNF causes intratumoral endothelial damage and blood supply disruption, which are associated with localized tumor cell death. Thus, intratumoral antigen-triggered T cell activation can mediate antitumor effects without direct recognition of living tumor cells, thereby avoiding many of the inhibitory mechanisms that limit anti-tumor immunity.

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Publication Details

Journal
Science
Published
2026-06-18
DOI
https://doi.org/10.1126/science.ads7910
Primary Topic
Immune cells in cancer
Type
article
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article

CD4 + T cells impair tumor growth through IL-3 and TNF-dependent vascular damage

Michael C. Kelly, Waipan Chan, Rémy Bosselut, Mariah Balmaceno-Criss et al.
Science
Immune cells in cancer
article

CD4 + T cells impair tumor growth through IL-3 and TNF-dependent vascular damage

Michael C. Kelly, Waipan Chan, Rémy Bosselut, Mariah Balmaceno-Criss, Alexander D. Clark, Melanie S. Vacchio, Weiming Yu, Elijah F. Edmondson, Qiaoshi Lian, Ronald N. Germain, Jatinder Singh, Qiang Chen, Jia Nie, Jennifer Matta
article en

Abstract

Most cancer immunotherapy strategies are focused on direct tumor killing by immune cells, especially T lymphocytes. Clinical and conceptual limitations of these approaches create a need for additional strategies. We identified a tumor stroma–targeting mechanism in which tumor antigen–specific CD4 + T cells inhibit tumor growth through myeloid cell and tumor necrosis factor (TNF)–dependent vascular damage. Multiplex immunofluorescence and single-cell and tissue transcriptomics showed that CD4 + T cells trigger the formation of perivascular myeloid cell clusters containing “classically activated” macrophages that produce TNF in response to T cell–derived interleukin-3. TNF causes intratumoral endothelial damage and blood supply disruption, which are associated with localized tumor cell death. Thus, intratumoral antigen-triggered T cell activation can mediate antitumor effects without direct recognition of living tumor cells, thereby avoiding many of the inhibitory mechanisms that limit anti-tumor immunity.

ScienceVol. 392(6804)
National Institutes of Health (US), Frederick National Laboratory for Cancer Research (US), National Institute of Allergy and Infectious Diseases (US), National Cancer Institute (US)
Good health and well-being
Openalex Percentile: Top 9%
Immune cells in cancer
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