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Interaction of glioma-associated microglia/macrophages and anti-PD1 immunotherapy
in
Antibodies
/ Antigens
/ Apoptosis
/ Brain cancer
/ Brain research
/ CD4 antigen
/ Cloning
/ Genotype & phenotype
/ Glioma
/ Growth factors
/ Immunology
/ Immunotherapy
/ Laboratory animals
/ Ligands
/ Lymphocytes
/ Lymphocytes T
/ Macrophages
/ Medical research
/ Microenvironments
/ Microglia
/ Nitric oxide
/ PD-1 protein
/ PD-L1 protein
/ Phenotypes
/ Proteins
/ Tumor necrosis factor-TNF
/ Tumors
2023
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Interaction of glioma-associated microglia/macrophages and anti-PD1 immunotherapy
by
in
Antibodies
/ Antigens
/ Apoptosis
/ Brain cancer
/ Brain research
/ CD4 antigen
/ Cloning
/ Genotype & phenotype
/ Glioma
/ Growth factors
/ Immunology
/ Immunotherapy
/ Laboratory animals
/ Ligands
/ Lymphocytes
/ Lymphocytes T
/ Macrophages
/ Medical research
/ Microenvironments
/ Microglia
/ Nitric oxide
/ PD-1 protein
/ PD-L1 protein
/ Phenotypes
/ Proteins
/ Tumor necrosis factor-TNF
/ Tumors
2023
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Interaction of glioma-associated microglia/macrophages and anti-PD1 immunotherapy
in
Antibodies
/ Antigens
/ Apoptosis
/ Brain cancer
/ Brain research
/ CD4 antigen
/ Cloning
/ Genotype & phenotype
/ Glioma
/ Growth factors
/ Immunology
/ Immunotherapy
/ Laboratory animals
/ Ligands
/ Lymphocytes
/ Lymphocytes T
/ Macrophages
/ Medical research
/ Microenvironments
/ Microglia
/ Nitric oxide
/ PD-1 protein
/ PD-L1 protein
/ Phenotypes
/ Proteins
/ Tumor necrosis factor-TNF
/ Tumors
2023
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Interaction of glioma-associated microglia/macrophages and anti-PD1 immunotherapy
Journal Article
Interaction of glioma-associated microglia/macrophages and anti-PD1 immunotherapy
2023
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Overview
Anti-PD-1-based therapy has resulted in a minimal clinical response in malignant gliomas. Gliomas contain numerous glioma-associated microglia/macrophages (GAMs), reported to contribute to an immunosuppressive microenvironment and promote glioma progression. However, whether and how GAMs affect anti-PD-1 immunotherapy in glioma remains unclear. Here, we demonstrated that M1-like GAMs contribute to the anti-PD-1 therapeutic response, while the accumulation of M2-like GAMs is associated with therapeutic resistance. Furthermore, we found that PD-L1 ablation reverses GAMs M2-like phenotype and is beneficial to anti-PD-1 therapy. We also demonstrated that tumor-induced impairment of the antigen-presenting function of GAMs could limit the antitumor immunity of CD4+ T cells in anti-PD-1 therapy. Our study highlights the impact of GAMs activation on anti-PD-1 treatment and provides new insights into the role of GAMs in regulating anti-PD-1 therapy in gliomas.
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