ArticleBMC medicine2026
Myeloid-derived immunosuppression of chimeric antigen receptor T cells in the neuronal microenvironment of glioblastoma.
Article in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- The immunosuppressive tumor microenvironment in glioblastoma.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChimeric antigen receptor (CAR)-T cell therapy remains largely ineffective in glioblastoma (GB), where a highly immunosuppressive microenvironment and tumor heterogeneity impair therapeutic durability.
methodsUsing a human neocortical brain slice model that preserves the complex GB microenvironment, we profiled interactions between natural killer group 2D (NKG2D) CAR-T cells and tumor ecosystems via PIC-seq, spatial transcriptomics, and gene regulatory network reconstruction.
resultsCAR-T cells showed an early but unsustained tumor-suppressive effect in the slice model. Single-cell profiling revealed that CAR CD8 T cells adopt an effector-skewed activation state accompanied by coordinated upregulation of checkpoint receptors and an exhaustion-associated transcription factor program. These transcriptional changes were linked to ligand-receptor signaling interactions between CAR-T cells and myeloid populations. Tumor-associated macrophages displayed enhanced phagocytic programs and spatially co-localized with mesenchymal-like GB cells within hypoxic regions. Gene regulatory network analysis identified MAF and BACH2 as candidate regulators of CD8 T cell state, with MAF enriched in CAR CD8 T cells exhibiting exhaustion-like features, and BACH2 enriched in Mock CD8 T cells consistent with less differentiated programs. In silico perturbation analyses further suggested a reciprocal effect of MAF and BACH2 on CD8 T cell transcriptional trajectories.
conclusionsThese data map the microenvironmental and transcriptional changes associated with rapid CAR-T cell dysfunction in GB and identify candidate pathways and regulators that may be leveraged to engineer more durable cellular therapies.
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