ReviewFrontiers in immunology2026
Metabolic immune checkpoints in cancer: how tumor-derived metabolites shape immunotherapy resistance.
Review in Frontiers in immunology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
Immune checkpoint blockade has transformed cancer therapy, yet many tumors remain intrinsically resistant or acquire resistance after initial response. Increasing evidence indicates that this failure is not determined solely by PD-1, PD-L1, CTLA-4, or T-cell exhaustion, but also by metabolically suppressive states within the tumor microenvironment. Tumor-derived metabolites can function as metabolic immune checkpoints by limiting effector immune activity, promoting regulatory or myeloid suppressive compartments, and weakening immunotherapy efficacy. This mini review summarizes recent experimental evidence showing how lactate, adenosine, tryptophan-derived metabolites, and nucleotide-derived metabolites shape immune escape and resistance to immune checkpoint blockade. Lactate links tumor glycolysis to Treg recruitment, impaired T-cell function, and lactylation-associated therapeutic resistance. The CD73-adenosine axis suppresses CD8
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