ArticleJournal for immunotherapy of cancer2026
N-glycans in non-malignant tumor microenvironment cells dampen CAR-T cell function in solid tumors.
Article in Journal for immunotherapy of cancer, 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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Abstract
backgroundChimeric antigen receptor (CAR) T-cell therapy has shown limited efficacy in solid tumors, largely due to immunosuppressive mechanisms within the tumor microenvironment (TME). While tumor-associated glycans are known to protect malignant cells from immune attack, the contribution of N-glycans expressed by non-malignant TME populations to CAR-T cell dysfunction remains poorly defined.
methodsWe investigated the role of N-glycans in non-malignant TME populations, focusing on M2-like macrophages and hepatic stellate cells in liver metastasis of colorectal (CRC) and pancreatic cancer (PDAC). Using in vitro co-culture systems, transcriptomic analysis, and tumor-bearing humanized mouse models, we assessed how pharmacologic or genetic disruption of key nodes of the N-glycosylation pathway (
resultsIn patient samples, a branched N-glycan signature was associated with transcriptional programs characteristic of tumor-promoting macrophages and stromal cells, linking N-glycosylation to an immunosuppressive TME. Disruption of N-glycan synthesis in non-malignant TME cells reduced their immunosuppressive and tumor-supporting functions. Single-cell RNA sequencing of tumor-bearing humanized mice showed depletion of protumor IL1β
conclusionsThese findings show that N-glycans expressed by non-malignant TME cells restrain CAR-T cell responses in CRC and PDAC, highlighting
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