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Clinical and conceptual limitations of these approaches create a need for additional strategies. We identified a tumor stroma\u2013targeting mechanism in which tumor antigen\u2013specific CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells inhibit tumor growth through myeloid cell and tumor necrosis factor (TNF)\u2013dependent vascular damage. Multiplex immunofluorescence and single-cell and tissue transcriptomics showed that CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells trigger the formation of perivascular myeloid cell clusters containing \u201cclassically activated\u201d macrophages that produce TNF in response to T cell\u2013derived 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.\n                  <\/jats:p>","DOI":"10.1126\/science.ads7910","type":"journal-article","created":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T18:03:22Z","timestamp":1781805802000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":3,"title":["CD4\n                    <sup>+<\/sup>\n                    T cells impair tumor growth through IL-3 and TNF-dependent vascular damage"],"prefix":"10.1126","volume":"392","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3628-9390","authenticated-orcid":true,"given":"Qiaoshi","family":"Lian","sequence":"first","affiliation":[{"name":"Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National 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