Tumor-associated microglia and macrophages (TAM) make up the largest immune cell population in the glioblastoma (GBM) tumor microenvironment. Given the heterogeneity and plasticity of TAMs in the GBM tumor microenvironment, understanding the context-dependent cancer cell–TAM symbiotic interaction is crucial for understanding GBM biology and developing effective therapies. In a recent issue of Cell, Kloosterman and colleagues identified a subpopulation of glycoprotein nonmetastatic melanoma protein Bhigh lipid-laden microglia and macrophages (LLM) in GBM. Mesenchymal-like GBM cells help generate the LLM phenotype. Reciprocally, LLMs are epigenetically rewired to recycle myelin and transfer the lipid from myelin to cancer cells, fueling mesenchymal-like GBM progression in a liver X receptor/ABCA1-dependent manner. Together, leveraging LLMs opens new therapeutic possibilities for rewiring the metabolism-mediated tumor–TAM interaction during GBM progression.

中文翻译：

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富含脂质的巨噬细胞回收髓鞘以喂养胶质母细胞瘤


肿瘤相关小胶质细胞和巨噬细胞 （TAM） 构成了胶质母细胞瘤 （GBM） 肿瘤微环境中最大的免疫细胞群。鉴于 TAM 在 GBM 肿瘤微环境中的异质性和可塑性，了解环境依赖性癌细胞-TAM 共生相互作用对于理解 GBM 生物学和开发有效疗法至关重要。在最近一期的《细胞》杂志上，Kloosterman 及其同事在 GBM 中鉴定了糖蛋白非转移性黑色素瘤蛋白 B 高脂质小胶质细胞和巨噬细胞 （LLM。间充质样 GBM 细胞有助于产生 LLM 表型。反过来，LLMs 通过表观遗传重新连接以回收髓鞘并将脂质从髓鞘转移到癌细胞，以肝脏 X 受体/ABCA1 依赖性方式推动间充质样 GBM 进展。总之，利用 LLMs 为 GBM 进展期间重新连接代谢介导的肿瘤-TAM 相互作用开辟了新的治疗可能性。