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Regulatory T cell depletion promotes myeloid cell activation and glioblastoma response to anti-PD1 and tumor-targeting antibodies
Glioblastoma is invariably lethal and responds poorly to immune checkpoint blockade. Here, we examined the impact of regulatory T (Treg) cell depletion on glioblastoma progression and immunotherapy responsiveness. In human glioblastoma, elevated Treg cell signatures correlated with poorer survival outcomes, with these cells expressing high levels of CD25. In Nf1−/−Pten−/−EGFRvIII+ glioblastoma-bearing mice, a single dose of non-interleukin-2 (IL-2) blocking (NIB) anti-CD25 (anti-CD25NIB) antibody depleted Treg cells and promoted CD8+ T cell clonal expansion and partial tumor control, further enhanced by programmed cell death-1 (PD1)-blockade. Treg cell depletion induced interferon-γ (IFN-γ)-dependent tumor microenvironment remodeling, increasing Fcγ receptor (FcγR) expression on intratumoral myeloid cells and enhancing phagocytosis. Combination of anti-CD25NIB with anti-EGFRvIII tumor-targeting antibodies resulted in complete tumor control. Anti-human CD25NIB treatment of glioblastoma patient-derived tumor fragments effectively depleted Treg cells and activated CD8+ T cells. These findings underscore the therapeutic relevance of Treg targeting in glioblastoma and unveil potent combination strategies for anti-CD25NIB based on innate cell activation.
Date:
19 November 2025, 16:00
Venue:
Venue to be announced
Speaker:
Dr. Felipe Galvez-Cancino (Centre for Immuno-oncology, University of Oxford)
Organising department:
Wellcome Trust Centre for Human Genetics
Organiser:
Dr Eoghan Mulholland (University of Oxford)
Organiser contact email address:
eoghan.mulholland@well.ox.ac.uk
Part of:
GO-PRECiSE Seminar Series (GPS)
Booking required?:
Recommended
Audience:
Public
Editors:
Eoghan Mulholland,
Jessica Taplin
