Reprogramming the breast tumor immune microenvironment: cold-to-hot transition for enhanced immunotherapy DOI Creative Commons
Saber Imani, Reyhaneh Farghadani, Ghazaal Roozitalab

et al.

Journal of Experimental & Clinical Cancer Research, Journal Year: 2025, Volume and Issue: 44(1)

Published: April 25, 2025

Abstract This review discusses reprogramming the breast tumor immune microenvironment from an immunosuppressive cold state to immunologically active hot state. A complex interplay is revealed, in which accumulation of metabolic byproducts—such as lactate, reactive oxygen species (ROS), and ammonia—is shown impair T-cell function promote escape. It demonstrated that (TME) dominated by cytokines, including interleukin-10 (IL-10), transforming growth factorβ (TGFβ), IL-35. Notably, IL-35 produced regulatory T cells cancer cells. The conversion conventional into IL-35-producing induced cells, along with inhibition pro-inflammatory cytokine secretion, contributes suppression anti-tumor immunity. further key checkpoint molecules—such PD-1, PDL1, CTLA-4, TIM-3, LAG-3, TIGIT—are upregulated within TME, leading Tcell exhaustion diminished responses. blockade these checkpoints restore functionality proposed a strategy convert tumors ones robust effector cell infiltration. therapeutic potential chimeric antigen receptor (CAR)T therapy also explored, targeting specific tumor-associated antigens, such glycoproteins tyrosine kinases, highlighted. suggested CART efficacy can be enhanced combining inhibitors other immunomodulatory agents, thereby overcoming barriers imposed TME. Moreover, role microbiome regulating estrogen metabolism systemic inflammation reviewed. Alterations gut microbiota are affect microbiome-based interventions additional means facilitate cold-to-hot transition. concluded immunological pathways underpin suppression—through combination strategies involving blockade, therapies, modulation—the TME achieved. anticipated enhance infiltration function, improving overall immunotherapies better clinical outcomes for patients.

Language: Английский

Reprogramming the breast tumor immune microenvironment: cold-to-hot transition for enhanced immunotherapy DOI Creative Commons
Saber Imani, Reyhaneh Farghadani, Ghazaal Roozitalab

et al.

Journal of Experimental & Clinical Cancer Research, Journal Year: 2025, Volume and Issue: 44(1)

Published: April 25, 2025

Abstract This review discusses reprogramming the breast tumor immune microenvironment from an immunosuppressive cold state to immunologically active hot state. A complex interplay is revealed, in which accumulation of metabolic byproducts—such as lactate, reactive oxygen species (ROS), and ammonia—is shown impair T-cell function promote escape. It demonstrated that (TME) dominated by cytokines, including interleukin-10 (IL-10), transforming growth factorβ (TGFβ), IL-35. Notably, IL-35 produced regulatory T cells cancer cells. The conversion conventional into IL-35-producing induced cells, along with inhibition pro-inflammatory cytokine secretion, contributes suppression anti-tumor immunity. further key checkpoint molecules—such PD-1, PDL1, CTLA-4, TIM-3, LAG-3, TIGIT—are upregulated within TME, leading Tcell exhaustion diminished responses. blockade these checkpoints restore functionality proposed a strategy convert tumors ones robust effector cell infiltration. therapeutic potential chimeric antigen receptor (CAR)T therapy also explored, targeting specific tumor-associated antigens, such glycoproteins tyrosine kinases, highlighted. suggested CART efficacy can be enhanced combining inhibitors other immunomodulatory agents, thereby overcoming barriers imposed TME. Moreover, role microbiome regulating estrogen metabolism systemic inflammation reviewed. Alterations gut microbiota are affect microbiome-based interventions additional means facilitate cold-to-hot transition. concluded immunological pathways underpin suppression—through combination strategies involving blockade, therapies, modulation—the TME achieved. anticipated enhance infiltration function, improving overall immunotherapies better clinical outcomes for patients.

Language: Английский

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