Authors
Abhirami P Suresh, Huikang Qian, Vinayak Uppin, Abhirami Thumsi, Da Sun, Madhan Mohan Chandra Sekhar Jaggarapu, Joslyn Mangal, Sahil Inamdar, Zheng-Rong Lu, Reshmi Parameswaran, Abhinav P Acharya
Published in
Journal of materials chemistry. B. Aug 17, 2026. Epub Aug 17, 2026.
Abstract
While chimeric antigen receptor (CAR)-T cell therapy has demonstrated remarkable clinical efficacy in hematological malignancies, its impact on solid tumors remains limited, largely due to insufficient T cell infiltration into the tumor microenvironment (TME). In contrast, macrophages are inherently recruited to the TME, offering a promising platform for cell-based immunotherapy. However, the nutrient-deprived conditions within the TME drive macrophages toward an immunosuppressive, tumor-promoting phenotype, thereby constraining their therapeutic potential. Here, we report a metabolic accelerating strategy designed to potentiate the anti-tumor activity of CAR-engineered macrophages (CAR-macs) by increasing their glycolytic capacity. We demonstrate that pre-treatment of CAR-macs with microparticles generated from fructose 1,6-bisphosphate (F16BP) can augment glycolytic flux and promote pro-inflammatory polarization. In a murine lymphoma solid tumor model, this approach significantly enhances anti-tumor immune cell responses and demonstrates that the CAR-macs are able to home to the tumor site. Our findings establish a novel paradigm in CAR macrophage-based immunotherapy, demonstrating that metabolic reprogramming can overcome the immunosuppressive TME and substantially improve therapeutic efficacy against solid tumors.
PMID:
42605790
Bibliographic data and abstract were imported from PubMed on 17 Aug 2026.
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