JZUS - Journal of Zhejiang University SCIENCE

Journal of Zhejiang University SCIENCE B

Accepted manuscript available online (unedited version)

Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies

Author(s): Shan WANG^1, ^2, Yage FU^1, ^2, Yamei HUANG¹
Affiliation(s): ¹Department of Oral Pathology, School of Stomatology, Hainan Medical University, Haikou 571199, China ²Department of Stomatology, The Second Affiliated Hospital of Hainan Medical University, Haikou 570216, China
Corresponding email(s): Shan WANG, birchtree20032003@126.com
Key Words: Tumor Immunotherapy; Macrophage Polarization; Immune Checkpoint Regulation; Metabolic Reprogramming; Combined Therapy Strategies

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Shan WANG^1,^2*, Yage FU^1,^2*, Yamei HUANG¹. Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org//10.1631/jzus.B2500179

@article{title="Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies",
author="Shan WANG^1,^2*, Yage FU^1,^2*, Yamei HUANG¹",
journal="Journal of Zhejiang University Science B",
year="in press",
publisher="Zhejiang University Press & Springer",
doi="https://doi.org//10.1631/jzus.B2500179"
}

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%A Yamei HUANG¹
%J Journal of Zhejiang University SCIENCE B
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doi="https://doi.org//10.1631/jzus.B2500179"

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T1 - Roles of macrophages in tumor immunotherapy: metabolism, immune checkpoints, and combination strategies
A1 - Shan WANG^{1
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A1 - Yamei HUANG¹
J0 - Journal of Zhejiang University Science B
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doi="https://doi.org//10.1631/jzus.B2500179"

Abstract
Chinese Summary
Academic Network
Reviewer Comment

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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