ArticleThe Journal of clinical investigation2026
CD8+ T cells in the tumor microenvironment modulate the response to endocrine therapy in breast cancer.
Article in The Journal of clinical investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- CXCL11 recruits immunosuppressive cells to form a barrier at the invasive front of pancreatic cancer by activating the NF-κB/CCL2 axis.Translational oncology · 2026Article
- Hydroxysafflor Yellow A Attenuates Sepsis-Induced Cardiac Dysfunction by Inhibiting Ferroptosis via Activation of Thioredoxin.Cardiovascular toxicology · 2026Article
- Targeting CB1 and TRPM8 receptors to counteract CD8+ T cell exhaustion.Scientific reports · 2026Article
- Unraveling TIME: CD8+ T cell- and CXCL11-driven endocrine resistance in breast cancer.The Journal of clinical investigation · 2026Article
- Therapeutic potential and mechanisms of rehabilitation interventions in preventing cancer metastasis.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
31 authors.
Funding
Abstract
The role of the tumor immune microenvironment (TIME) in modulating responses to antiestrogen therapy in hormone receptor-positive (HR+) breast cancers remains unclear. We analyzed pre- and on-treatment biopsies from patients with HR+ breast cancer treated with letrozole to induce estrogen deprivation (ED). Stromal tumor-infiltrating lymphocytes, assessed by H&E staining, and immune-related gene sets, including IFN-γ signaling genes, measured by RNA-Seq, were increased in ED-resistant tumors. Cyclic immunofluorescence and spatial transcriptomics revealed an abundance of CD8+ T cells and enhanced antigen processing and immune gene signatures in ED-resistant tumors. In this group, the expression of CXCL9, CXCL10, and CXCL11 - chemokine genes involved in CD8+ T cell recruitment - and the CXCR3 receptor were upregulated both before and after letrozole treatment. CXCL11 levels were higher in conditioned media from HR+ breast cancer cells cocultured with CD8+ T cells. Both recombinant CXCL11 and coculture with CD8+ T cells promoted MCF7 and T47D cell growth in estrogen-free conditions. Finally, deletion combined with silencing of the CXCL11 receptors CXCR3 and CXCR7 in MCF7 cells impaired proliferation in response to exogenous CXCL11 and to coculture with CD8+ T cells in estrogen-free conditions. These findings suggest that CD8+ T cell-associated CXCL11 in the TIME modulated the response of HR+ breast cancer cells to estrogen suppression.
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Registered trials
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