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Life sciences · Journal article
Biology Direct · October 11, 2026
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Glioblastoma (GBM) exhibits poor responsiveness to immune checkpoint blockade, largely due to an immunosuppressive tumor immune microenvironment. Tumor-associated macrophage (TAM) polarization critically regulates antitumor immunity, yet the role of human leukocyte antigen class II, DM alpha (HLA-DMA) in GBM remains elusive. Transcriptomic screening combined with The Cancer Genome Atlas (TCGA)-based bioinformatics and CIBERSORT immune-infiltration analysis was used to identify and characterize HLA-DMA. Loss-of-function assays were performed in U373MG and U87 cells to assess proliferation, apoptosis, migration, invasion, and AKT/mTOR signaling. A glioma-macrophage co-culture system, a subcutaneous syngeneic GBM model with or without anti-PD-1 treatment, and clinical glioma specimens were employed for immune and translational validation. HLA-DMA was overexpressed in GBM relative to low-grade glioma (LGG), positively correlated with IFI30 expression, predicted poor prognosis, and showed diagnostic value for glioma grading (AUC = 0.822). CIBERSORT analysis further showed that HLA-DMA expression was positively associated with M2 macrophage infiltration. HLA-DMA knockdown suppressed GBM cell proliferation, migration, and invasion, promoted apoptosis, and was accompanied by reduced AKT and mTOR phosphorylation. In co-culture, HLA-DMA knockdown shifted macrophages from an M2-like toward an M1-like phenotype, enhanced macrophage phagocytosis, increased TNF-α secretion, and decreased IL-10 release. In a subcutaneous GL261 model, knockdown of the murine ortholog H2-DMa inhibited tumor growth, increased CD8⁺ T-cell infiltration, and augmented the antitumor efficacy of anti-PD-1 therapy. HLA-DMA depletion suppresses malignant glioma phenotypes and promotes pro-inflammatory macrophage remodeling, while H2-DMa knockdown enhances anti-PD-1 response in vivo. These convergent tumor-intrinsic and immune findings position HLA-DMA/H2-DMa as a candidate therapeutic target for GBM immune-microenvironment remodeling.