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

Q Qiaoshi Lian (Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.) J Jia Nie J Jatinder Singh (Single Cell Analysis Facility, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.) Q Qiang Chen J Jennifer Matta (Molecular Histopathology Laboratory, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.) W Waipan Chan (Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.) M Mariah Balmaceno-Criss (Laboratory of Immune Cell Biology and Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.) M Melanie S. Vacchio (Laboratory of Immune Cell Biology and Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.) W Weiming Yu (Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.) A Alexander D. Clark (Laboratory of Immune Cell Biology and Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.) E Elijah Edmondson (Molecular Histopathology Laboratory, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.) M Michael C. Kelly (Single Cell Analysis Facility, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.) R Ronald N. Germain R Rémy Bosselut

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.

Article Details

Journal Science
Volume / Issue Vol. 392, Issue 6804
Published June 18, 2026
ISSN 0036-8075
Publisher American Association for the Advancement of Science

Journal Info

Science

American Association for the Advancement of Science

ISSN: 0036-8075 Social Sciences

Authors (14)

Q

Qiaoshi Lian

Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

J

Jia Nie

J

Jatinder Singh

Single Cell Analysis Facility, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Q

Qiang Chen

J

Jennifer Matta

Molecular Histopathology Laboratory, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

W

Waipan Chan

Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

M

Mariah Balmaceno-Criss

Laboratory of Immune Cell Biology and Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

M

Melanie S. Vacchio

Laboratory of Immune Cell Biology and Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

W

Weiming Yu

Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

A

Alexander D. Clark

Laboratory of Immune Cell Biology and Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

E

Elijah Edmondson

Molecular Histopathology Laboratory, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

M

Michael C. Kelly

Single Cell Analysis Facility, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

R

Ronald N. Germain

R

Rémy Bosselut