Phenotypic plasticity of myeloid cells in glioblastoma development, progression, and therapeutics

• Published in: Oncogene Vol. 40; no. 42; pp. 6059 - 6070
• Main Authors: Ye, Zengpanpan, Ai, Xiaolin, Zhao, Linjie, Fei, Fan, Wang, Ping, Zhou, Shengtao
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 21.10.2021; Nature Publishing Group
• Subjects: 13/21; 631/67/1059/602; 631/67/2329; Animals; Apoptosis; Blood cells; Brain cancer; Brain Neoplasms - drug therapy; Brain Neoplasms - immunology; Brain Neoplasms - pathology; Cancer; Care and treatment; Cell Biology; Development and progression; Disease Progression; Drug development; Drug therapy; Glioblastoma; Glioblastoma - drug therapy; Glioblastoma - immunology; Glioblastoma - pathology; Glioblastoma multiforme; Health aspects; Human Genetics; Humans; Immune Checkpoint Inhibitors - pharmacology; Immune Checkpoint Inhibitors - therapeutic use; Immunity, Innate; Immunostimulation; Immunotherapy; Innate immunity; Internal Medicine; Lymphocytes T; Macrophages; Medicine; Medicine & Public Health; Microglia; Myeloid cells; Myeloid Cells - drug effects; Myeloid Cells - immunology; Myeloid Cells - pathology; Oncology; Patients; Phenotype; Phenotypes; Phenotypic plasticity; Physiological aspects; Prognosis; Review Article; Tumor cells; Tumor Microenvironment; Tumor-infiltrating lymphocytes; China
• ISSN: 0950-9232; 1476-5594
• DOI: 10.1038/s41388-021-02010-1

Glioblastoma (GBM) is the most common and malignant type of intracranial tumors with poor prognosis. Accumulating evidence suggests that phenotypic alterations of infiltrating myeloid cells in the tumor microenvironment are important for GBM progression. Conventional tumor immunotherapy commonly targets T-cells, while innate immunity as a therapeutic target is an emerging field. Targeting infiltrating myeloid cells that induce immune suppression in the TME provides a novel direction to improve the prognosis of patients with GBM. The factors released by tumor cells recruit myeloid cells into tumor bed and reprogram infiltrating myeloid cells into immunostimulatory/immunosuppressive phenotypes. Reciprocally, infiltrating myeloid cells, especially microglia/macrophages, regulate GBM progression and affect therapeutic efficacy. Herein, we revisited biological characteristics and functions of infiltrating myeloid cells and discussed the recent advances in immunotherapies targeting infiltrating myeloid cells in GBM. With an evolving understanding of the complex interactions between infiltrating myeloid cells and tumor cells in the tumor microenvironment, we will expand novel immunotherapeutic regimens targeting infiltrating myeloid cells in GBM treatment and improve the outcomes of GBM patients.