ArticleCancer research2026
CCL5 hiCD4+ T Cells Regulate Macrophage Polarization and Promote Immunotherapy Response in Bladder Cancer.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Immune checkpoint inhibitors (ICI) have transformed cancer therapy, yet their efficacy remains limited to a subset of patients, underscoring the need for robust predictive biomarkers and deeper mechanistic insights into treatment resistance. In this study, we identified a population of CCL5hiCD4+ T cells that were characterized by memory-like activation markers and strongly correlated with ICI therapeutic responses in bladder cancer. Functionally, these T cells enhanced antitumor immunity by promoting M1-like macrophage polarization through CCL5/CCR1 signaling. Importantly, tumor-derived prostaglandin E2 (PGE2) acted as a critical microenvironmental factor that suppressed the differentiation of CCR6hiCD4+ T cells into immunostimulatory CCL5hiCD4+ T cells, thereby driving resistance to ICI therapy. These findings extend the understanding of CD4+ T-cell heterogeneity and its role in shaping immune responses to ICI. By elucidating that CCL5hiCD4+ T cells enhance myeloid-mediated tumor control and that tumor-derived PGE2 disrupts CCL5hiCD4+ T-cell differentiation to promote immune evasion, this work highlights potential therapeutic strategies to improve ICI efficacy in bladder cancer. SIGNIFICANCE: CCL5 hiCD4+ T cells with memory-like activated characteristics enhance antitumor immunity in bladder cancer by reprogramming macrophages, supporting the potential of these cells as biomarkers and targets to enhance immunotherapy efficacy.
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