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.
Journal article
2025-05-01T00:00:00+00:00
58
1236 - 1253.e8
Immune Regulation and Tumour Immunotherapy Laboratory, Cancer Immunology Unit, Research Department of Haematology, UCL Cancer Institute, University College London, London WC1E 6DD, UK; Immune Regulation Laboratory, Centre for Immuno-Oncology, Nuffield Department of Medicine, University of Oxford, Oxford, UK. Electronic address: felipe.galvez-cancino@immonc.ox.ac.uk.
CD8-Positive T-Lymphocytes, Cell Line, Tumor, Myeloid Cells, Animals, Mice, Knockout, Humans, Mice, Glioblastoma, Brain Neoplasms, Receptors, IgG, Antibodies, Monoclonal, Immunotherapy, Lymphocyte Depletion, Lymphocyte Activation, T-Lymphocytes, Regulatory, Interleukin-2 Receptor alpha Subunit, Tumor Microenvironment, Programmed Cell Death 1 Receptor, ErbB Receptors, Immune Checkpoint Inhibitors