Department of Experimental Medicine, University of Perugia, Polo Unico Sant'Andrea delle Fratte, Piazzale Gambuli, 06132 Perugia, Italy,,
Department of Chemistry, Biology and Biotechnology, Via Elce di sotto, 06123, Perugia, Italy.
Front Biosci (Landmark Ed). 2017 Jan 1;22(2):268-309. doi: 10.2741/4486.
Glioblastoma (GBM) is the most malignant and aggressive among primary brain tumors, characterized by very low life expectancy. In vivo, glioma and glioblastoma in particular contain large numbers of immune cells (myeloid cells) such as microglia and tumour-infiltrating macrophages (or glioma associated macrophages). These glioma-infiltrating myeloid cells comprise up to 30% of total tumor mass and have been suggested to play several roles in glioma progression including proliferation, survival, motility and immunosuppression. Although tumor microglia and macrophages can acquire proinflammatory (M1) phenotype being capable of releasing proinflammatory cytokines, phagocytosing and presenting antigens, their effector immune function in gliomas appears to be suppressed by the acquisition of an anti-inflammatory (M2) phenotype. In the present work we review the microglia-glioma interactions to highlight the close relationship between the two cell types and the factors that can influence their properties (chemokines, cytokines, S100B protein). A future therapeutic possibility might be to simultaneously targeting, for example with nanomedicine, glioma cells and microglia to push the microglia towards an antitumor phenotype (M1) and/or prevent glioma cells from "conditioning" by microglia.
胶质母细胞瘤（GBM）是原发性脑肿瘤中最恶性和侵袭性的，其预期寿命非常低。在体内，神经胶质瘤，尤其是胶质母细胞瘤，含有大量的免疫细胞（髓样细胞），如小胶质细胞和肿瘤浸润巨噬细胞（或胶质母细胞瘤相关巨噬细胞）。这些浸润性髓样细胞占肿瘤总质量的 30%，被认为在神经胶质瘤的进展中发挥多种作用，包括增殖、存活、迁移和免疫抑制。尽管肿瘤小胶质细胞和巨噬细胞可以获得促炎（M1）表型，能够释放促炎细胞因子、吞噬和呈递抗原，但它们在神经胶质瘤中的效应免疫功能似乎受到获得抗炎（M2）表型的抑制。在本工作中，我们综述了小胶质细胞-神经胶质瘤的相互作用，以强调两种细胞类型之间的密切关系以及可以影响它们特性的因素（趋化因子、细胞因子、S100B 蛋白）。未来的治疗可能性可能是同时靶向，例如用纳米医学靶向，神经胶质瘤细胞和小胶质细胞，以推动小胶质细胞向抗肿瘤表型（M1）发展，和/或防止神经胶质瘤细胞被小胶质细胞“调节”。
