表皮生长因子受体（EGFR）是着丙酸钠化脑胶质瘤（GBM）中最常改变的基因，它在肿瘤发展和抗肿瘤免疫反应中起重要作用。虽然当前针对EGFR信号通路及其下游关键分子的分子靶向治疗在GBM的临床效果不佳。而免疫治疗，特别是免疫检查点抑制剂，在许多癌症中显示出持久的抗肿瘤反应。然而，在携带EGFR改变的患者中，临床疗效有限，表明EGFR信号可能涉及肿瘤免疫反应。最近的研究发现，EGFR改变不仅促进GBM细胞增殖，还影响肿瘤微环境（TME）中的免疫成分，导致免疫抑制细胞（如M2型肿瘤关联巨噬细胞、MDSC和Treg细胞）的招募以及T和NK细胞的抑制。此外，EGFR改变还上调了免疫抑制分子或细胞因子（如PD-L1、CD73、TGF-β）的表达。本综述探讨了EGFR改变在建立免疫抑制的TME中的作用，并希望为将靶向EGFR抑制剂与免疫治疗相结合治疗GBM提供理论依据。版权所有 © 2023 Li, Guo, Wang and Zhao.

The epidermal growth factor receptor (EGFR) is the most frequently altered gene in glioblastoma (GBM), which plays an important role in tumor development and anti-tumor immune response. While current molecular targeted therapies against the EGFR signaling pathway and its downstream key molecules have not demonstrated favorable clinical outcomes in GBM. Whereas tumor immunotherapies, especially immune checkpoint inhibitors, have shown durable antitumor responses in many cancers. However, the clinical efficacy is limited in patients carrying EGFR alterations, indicating that EGFR signaling may involve tumor immune response. Recent studies reveal that EGFR alterations not only promote GBM cell proliferation but also influence immune components in the tumor microenvironment (TME), leading to the recruitment of immunosuppressive cells (e.g., M2-like TAMs, MDSCs, and Tregs), and inhibition of T and NK cell activation. Moreover, EGFR alterations upregulate the expression of immunosuppressive molecules or cytokines (such as PD-L1, CD73, TGF-β). This review explores the role of EGFR alterations in establishing an immunosuppressive TME and hopes to provide a theoretical basis for combining targeted EGFR inhibitors with immunotherapy for GBM.Copyright © 2023 Li, Guo, Wang and Zhao.