IMR Press / FBL / Volume 30 / Issue 10 / DOI: 10.31083/FBL44810
Open Access Opinion
Beyond Passive Bystander: Glioblastoma-Educated Astrocyte Suppressing T Cell
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Affiliation
1 Institute of Cancer Neuroscience, Medical Frontier Innovation Research Center, The First Hospital of Lanzhou University, The First Clinical Medical College of Lanzhou University, 730000 Lanzhou, Gansu, China
2 School of Life Science, Lanzhou University, 730000 Lanzhou, Gansu, China
*Correspondence: ldyy_jinwl@lzu.edu.cn (Wei-Lin Jin)
Front. Biosci. (Landmark Ed) 2025, 30(10), 44810; https://doi.org/10.31083/FBL44810
Submitted: 11 July 2025 | Revised: 4 September 2025 | Accepted: 11 September 2025 | Published: 31 October 2025
Copyright: © 2025 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.
Abstract

Faust Akl et al. revealed in Nature a paradigm-shifting mechanism distinct from myeloid-driven immunosuppression, whereby glioblastoma induces T-cell apoptosis via tumor-derived IL-11, prompting astrocytes to reprogram into immunosuppressive tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)+ effectors, thereby establishing astrocytes as active immunomodulators. Therapeutically, herpes simplex virus type 1 (HSV-1) (anti-TRAIL) achieves a dual therapeutic effect, offering novel strategies to overcome glioblastoma (GBM)’s evasion tactics.

Keywords
astrocyte
IL-11
glioblastoma
oncolytic virus
STAT3
immune-suppressive TME
Funding
High Level Talent Introduction Funds from the First Hospital of Lanzhou University
Figures
Fig. 1.
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