Trp-Kyn enzymes are inducible by interferons and oncogenic cues and are distributed across malignant cells as well as cancer-associated fibroblasts, endothelial cells and tumor-associated myeloid populations, generating spatially restricted "Trp-low/Kyn-high" immunometabolic niches.
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Trp-low/Kyn-high immunometabolic niches
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Bulk, single-cell, and spatial multi-omics studies support that Trp-Kyn pathway activity in HNSCC is compartmentalized rather than uniform.
Within Trp-low/Kyn-high niches, tryptophan starvation and kynurenine-driven signaling suppress effector T-cell expansion, promote regulatory T-cell programs, undermine dendritic-cell priming, and reinforce tolerogenic myeloid states.
In HNSCC, Trp-Kyn enzymes are distributed across malignant cells, cancer-associated fibroblasts, endothelial cells, and tumor-associated myeloid populations, generating spatially restricted Trp-low/Kyn-high immunometabolic niches.
Trp-low/Kyn-high immunometabolic niches in HNSCC foster T-cell exhaustion and reduced sensitivity to PD-1/PD-L1 blockade.