ArticleJournal of translational medicine2025
ATP11B triggers the infiltration of T cells into GBM and intensifies anti-GBM immunity by upregulating and externalizing S1PR1.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Review
- ACT001 synergizes with temozolomide-based chemoradiotherapy to cure refractory glioblastoma by targeting TNF-CXCL10-CD8Frontiers in pharmacology · 2026Article
- Dysregulated arginine metabolism is associated with pro-tumor neutrophil polarization in liver cancer.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundInsufficient T-cell infiltration in tumours causes immune checkpoint inhibitor (ICI) resistance in glioblastoma (GBM) patients. The aim of this study was to demonstrate a preferable way to facilitate T-cell infiltration and improve the therapeutic effects of ICIs in GBM.
methodsFlow cytometry, western blot and immunofluorescence staining were used to detect the effects of ATP11B upregulation on S1PR1 expression and distribution, T-cell infiltration and differentiation. A coculture system and an intracranial GBM model were established to explore the anti-GBM potential of ATP11B/S1PR1 signaling through systemic administration of CD3-DSPE-PEG2K-NHS/ATP11B nanoparticles to specifically deliver ATP11B overexpressing plasmids to T cells.
resultsS1PR1 deficiency in T cells caused T-cell lymphopenia and systemic immunosuppression in GBM, whereas ATP11B overexpression induced the upregulation and externalization of S1PR1 on T-cell membranes, thus increasing the ability of T cells to eliminate GBM cells. In intracranial GBM models, an ATP11B overexpression plasmid was specifically delivered to T cells in the peripheral blood, bone marrow and spleen, then triggering the infiltration of T cells deeply into the GBM and reversing systemic immunosuppression, ultimately enhancing the therapeutic outcomes of ICIs.
conclusionsThe upregulation and externalization of S1PR1 on T cells mediated by ATP11B overexpression may be promising immunotherapeutic alternatives for GBM treatment.
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Registered trials
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