Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma

Abstract The immunosuppressive tumor microenvironment of glioblastoma limits the effectiveness of most immunotherapies. Transforming growth factor (TGF)-β signaling drives tumor progression and prevents effective T cell activity. Notably, both regulatory T cells (Tregs) and effector T cells within g...

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Main Authors: Daniela Lorizio, Manuela Silginer, Julia Friesen, Alan L. Epstein, Michael Weller, Patrick Roth
Format: Article
Language:English
Published: Springer 2025-06-01
Series:Cancer Immunology, Immunotherapy
Subjects:
Online Access:https://doi.org/10.1007/s00262-025-04098-w
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author Daniela Lorizio
Manuela Silginer
Julia Friesen
Alan L. Epstein
Michael Weller
Patrick Roth
author_facet Daniela Lorizio
Manuela Silginer
Julia Friesen
Alan L. Epstein
Michael Weller
Patrick Roth
author_sort Daniela Lorizio
collection DOAJ
description Abstract The immunosuppressive tumor microenvironment of glioblastoma limits the effectiveness of most immunotherapies. Transforming growth factor (TGF)-β signaling drives tumor progression and prevents effective T cell activity. Notably, both regulatory T cells (Tregs) and effector T cells within glioblastoma and other tumors express high levels of the immune checkpoint receptor, glucocorticoid-induced tumor necrosis factor receptor (GITR), which modulates T cell activation and function. Combining GITR agonism with TGF-β inhibition may therefore offer a compelling approach to restore anti-tumor immunity. We evaluated the combined effects of TGF-β inhibition and GITR modulation using two different GITR agonists in syngeneic mouse glioma models. GITR modulation enhanced T cell activation, as shown by increased cytokine secretion and effector T cell proliferation in vitro. Combining GITR modulation with TGF-β inhibition amplified these effects, resulting in significantly stronger immune cell-mediated tumor cell killing compared to single-agent treatments. Combination therapy improved survival of glioma-bearing mice, with a higher fraction of long-term survivors compared to monotherapy. Surviving mice resisted tumor re-challenge, indicating durable adaptive immunity. In summary, dual targeting of TGF-β and GITR pathways synergistically enhances anti-tumor immunity in glioblastoma. This novel combination strategy demonstrates clinical potential by addressing the limitations of existing immunotherapies and offering a promising approach for durable and effective glioblastoma treatment.
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spelling doaj-art-569baef96f114ad6b4db24dbf29f664f2025-08-20T03:42:53ZengSpringerCancer Immunology, Immunotherapy1432-08512025-06-0174811410.1007/s00262-025-04098-wSimultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in gliomaDaniela Lorizio0Manuela Silginer1Julia Friesen2Alan L. Epstein3Michael Weller4Patrick Roth5Department of Neurology and Brain Tumor Center, University Hospital Zurich and University of ZurichDepartment of Neurology and Brain Tumor Center, University Hospital Zurich and University of ZurichDepartment of Neurology and Brain Tumor Center, University Hospital Zurich and University of ZurichDepartment of Pathology, Keck School of Medicine, University of Southern CaliforniaDepartment of Neurology and Brain Tumor Center, University Hospital Zurich and University of ZurichDepartment of Neurology and Brain Tumor Center, University Hospital Zurich and University of ZurichAbstract The immunosuppressive tumor microenvironment of glioblastoma limits the effectiveness of most immunotherapies. Transforming growth factor (TGF)-β signaling drives tumor progression and prevents effective T cell activity. Notably, both regulatory T cells (Tregs) and effector T cells within glioblastoma and other tumors express high levels of the immune checkpoint receptor, glucocorticoid-induced tumor necrosis factor receptor (GITR), which modulates T cell activation and function. Combining GITR agonism with TGF-β inhibition may therefore offer a compelling approach to restore anti-tumor immunity. We evaluated the combined effects of TGF-β inhibition and GITR modulation using two different GITR agonists in syngeneic mouse glioma models. GITR modulation enhanced T cell activation, as shown by increased cytokine secretion and effector T cell proliferation in vitro. Combining GITR modulation with TGF-β inhibition amplified these effects, resulting in significantly stronger immune cell-mediated tumor cell killing compared to single-agent treatments. Combination therapy improved survival of glioma-bearing mice, with a higher fraction of long-term survivors compared to monotherapy. Surviving mice resisted tumor re-challenge, indicating durable adaptive immunity. In summary, dual targeting of TGF-β and GITR pathways synergistically enhances anti-tumor immunity in glioblastoma. This novel combination strategy demonstrates clinical potential by addressing the limitations of existing immunotherapies and offering a promising approach for durable and effective glioblastoma treatment.https://doi.org/10.1007/s00262-025-04098-wGlioblastomaGITRLMicroenvironmentImmunotherapyImmunosuppression
spellingShingle Daniela Lorizio
Manuela Silginer
Julia Friesen
Alan L. Epstein
Michael Weller
Patrick Roth
Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma
Cancer Immunology, Immunotherapy
Glioblastoma
GITRL
Microenvironment
Immunotherapy
Immunosuppression
title Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma
title_full Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma
title_fullStr Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma
title_full_unstemmed Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma
title_short Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma
title_sort simultaneous tgf β and gitr pathway modulation promotes anti tumor immunity in glioma
topic Glioblastoma
GITRL
Microenvironment
Immunotherapy
Immunosuppression
url https://doi.org/10.1007/s00262-025-04098-w
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