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Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies
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Shan WANG1,2*, Yage FU1,2*, Yamei HUANG1. Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .
@article{title="Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies",
author="Shan WANG1,2*, Yage FU1,2*, Yamei HUANG1",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="/10.1631/jzus.B2500179"
}
%0 Journal Article
%T Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies
%A Shan WANG1
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%A Yamei HUANG1
%J Journal of Zhejiang University SCIENCE B
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%@ 1673-1581
%D 1998
%I Zhejiang University Press & Springer
%DOI /10.1631/jzus.B2500179
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T1 - Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies
A1 - Shan WANG1
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A1 - Yamei HUANG1
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PB - Zhejiang University Press & Springer
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DOI - /10.1631/jzus.B2500179
Abstract: Macrophages influence antitumor immunity through tractable metabolic and checkpoint programs. Within hypoxic, nutrient-competitive tumor beds, tumor-associated macrophages (TAMs) adopt oxidative and lipid-based metabolisms, dampening antigen presentation and T-cell support. Converging evidence shows that lactate flux, fatty acid oxidation (FAO), and glutamine handling steer TAMs toward immunosuppressive states that blunt checkpoint efficacy. Here, we synthesize the mechanism by which discrete pathways-glycolysis/PPP switching, FAO-lysosomal lipolysis, and glutamine- α-ketoglutarate signaling-mechanistically reprogram TAMs. We then map these circuits onto combination strategies involving PD-(L)1/CTLA-4 blockade, chemotherapy/radiotherapy, and CAR-T. Rather than providing a catalogue, we emphasize when metabolic rewiring dominates, which TAM subsets are affected, and how these levers can be timed or co-inhibited to restore cytotoxic T-cell function. This approach provides operational guidance for pairing macrophage-directed agents with immune checkpoint inhibitors in solid tumors.
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