Cell Reports· 2025Q1· Review
Metabolic regulation of immunity in the tumor microenvironment
- 67citations
- Q1SCImago
- 2025year
Short summary
Tumor cells and immunosuppressive cells reprogram metabolism in the tumor microenvironment (TME), leading to nutrient competition, toxic metabolite buildup, and immune cell exhaustion, while tertiary lymphoid structures can support immune cell function.
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Key points
- Tumor cells reprogram metabolism, causing nutrient competition and toxic metabolite accumulation in the TME.
- Immunosuppressive cells display strong metabolic adaptability, reinforcing the suppressive TME.
- Tertiary lymphoid structures can act as nutrient-rich 'moats' supporting B and T cell functions.
- Metabolic-immune interactions form 'enzyme-metabolite-receptor' checkpoints that promote ICI resistance.
AI-generated from the title and abstract; the full text is not read.
Abstract
Metabolic-immune crosstalk in the tumor microenvironment (TME) is a critical driver of tumorigenesis, progression, and immune evasion. Tumor cells undergo profound metabolic reprogramming, causing nutrient competition, toxic metabolite accumulation, and the formation of cold niches that gradually exhaust effector immune cells. In contrast, immunosuppressive cells exhibit strong metabolic adaptability, reinforcing the suppressive milieu. Moreover, tertiary lymphoid structures provide nutrient- and oxygen-rich "moats" that sustain the functions of B and T cells. In addition, metabolic-immune interactions establish novel checkpoints through an "enzyme-metabolite-receptor" axis, which synergize with PD-1/CTLA-4 pathways to promote resistance to immune checkpoint inhibitors (ICIs). Although monotherapies with metabolic inhibitors have shown limited efficacy, their combination with ICIs is promising. Therefore, this review discusses the field from three perspectives: metabolic stress in the TME, immune cell adaptation, and targeting metabolic immune checkpoints in combination with immunotherapy.
The authors' abstract, as published at the source. Cell Reports, 2025 · DOI ↗
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