Gliomas, the most common type of primary brain tumor, are a significant cause of morbidity and mortality worldwide. Glioblastoma, a highly malignant subtype, is particularly common, aggressive, and resistant to treatment. The tumor microenvironment (TME) of gliomas, especially glioblastomas, is characterized by a distinct presence of tumor-associated macrophages (TAMs), which densely infiltrate glioblastomas, a hallmark of these tumors. This macrophage population comprises both tissue-resident microglia as well as macrophages derived from the walls of blood vessels and the blood stream. Ionized calcium-binding adapter molecule 1 (Iba1) and CD163 are established cellular markers that enable the identification and functional characterization of these cells within the TME. This review provides an in-depth examination of the roles of Iba1 and CD163 in malignant gliomas, with a focus on TAM activation, migration, and immunomodulatory functions. Additionally, we will discuss how recent advances in AI-enhanced cell identification and visualization techniques have begun to transform the analysis of TAMs, promising unprecedented precision in their characterization and providing new insights into their roles within the TME. Iba1 and CD163 appear to have both unique and shared roles in glioma pathobiology, and both have the potential to be targeted through different molecular and cellular mechanisms. We discuss the therapeutic potential of Iba1 and CD163 based on available preclinical (experimental) and clinical (human tissue-based) evidence.
胶质瘤作为最常见的原发性脑肿瘤,是全球范围内发病和死亡的重要原因。其中胶质母细胞瘤作为高度恶性的亚型,具有极高的发病率、侵袭性和治疗抵抗性。胶质瘤(特别是胶质母细胞瘤)的肿瘤微环境以大量肿瘤相关巨噬细胞的浸润为显著特征,这是该类肿瘤的标志性特点。该巨噬细胞群体既包含组织驻留的小胶质细胞,也包含来源于血管壁及血流的巨噬细胞。离子钙结合衔接分子1和CD163作为成熟的细胞标志物,可用于在肿瘤微环境中对这些细胞进行鉴定和功能表征。本综述深入探讨了Iba1和CD163在恶性胶质瘤中的作用,重点关注TAM的活化、迁移及免疫调节功能。同时,我们将讨论人工智能增强的细胞识别与可视化技术的最新进展如何开始改变TAM的分析方式,有望实现前所未有的精准表征,并为理解其在肿瘤微环境中的作用提供新见解。Iba1和CD163在胶质瘤病理生物学中既发挥独特作用又存在共同功能,两者都可能通过不同的分子和细胞机制成为治疗靶点。我们将基于现有的临床前(实验性)和临床(基于人体组织)证据,探讨Iba1和CD163的治疗潜力。
TAMing Gliomas: Unraveling the Roles of Iba1 and CD163 in Glioblastoma