Multidimensional plasticity of natural killer cells in tumours
Yang X., Song Z., Chen L., Jia Q., Li M.
Narrative Review, published in Cell Death Dis (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Cell Death Dis (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41429765
- PMCID
- PMC12749834
- DOI
- 10.1038/s41419-025-08361-x
Abstract (original English)
Natural killer (NK) cells exhibit remarkable adaptability within the tumour microenvironment (TME), where dynamic shifts in phenotype, function and metabolism govern their dual roles in antitumour immunity and tumour immune evasion. In the TME, NK cells undergo receptor remodelling, which is characterised by upregulated inhibitory signals and suppressed activating receptors, leading to the formation of dysfunctional subsets, such as exhausted TIM-3⁺ NK cells or tissue-resident CD49a⁺ populations. Immunosuppressive factors within the TME drive a transition from cytotoxic activity to regulatory or senescent-like states, impairing tumour surveillance. Metabolic reprogramming further compromises NK cell effector functions, as nutrient deprivation and metabolic byproducts disrupt energy pathways and suppress immune responses. Therapeutic strategies targeting this plasticity include engineered natural killer (NK) cells with enhanced specificity, metabolic restoration approaches and microenvironment-modulating interventions. However, challenges persist because of TME heterogeneity and persistent dysfunctional states. Understanding these adaptive mechanisms provides a framework for developing NK cell-based therapies that leverage plasticity to counteract tumour resistance.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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