Department of Neurosurgery, University of Minnesota, Minneapolis, MN 55455, USA.
Int J Mol Sci. 2021 May 28;22(11):5775. doi: 10.3390/ijms22115775.
The complex interaction between glioblastoma and its microenvironment has been recognized for decades. Among various immune profiles, the major population is tumor-associated macrophage, with microglia as its localized homolog. The present definition of such myeloid cells is based on a series of cell markers. These good sentinel cells experience significant changes, facilitating glioblastoma development and protecting it from therapeutic treatments. Huge, complicated mechanisms are involved during the overall processes. A lot of effort has been dedicated to crack the mysterious codes in macrophage/microglia recruiting, activating, reprogramming, and functioning. We have made our path. With more and more key factors identified, a lot of new therapeutic methods could be explored to break the ominous loop, to enhance tumor sensitivity to treatments, and to improve the prognosis of glioblastoma patients. However, it might be a synergistic system rather than a series of clear, stepwise events. There are still significant challenges before the light of truth can shine onto the field. Here, we summarize recent advances in this field, reviewing the path we have been on and where we are now.
几十年来,人们已经认识到胶质母细胞瘤与其微环境之间的复杂相互作用。在各种免疫特征中,主要群体是肿瘤相关巨噬细胞,其局部同源物是小胶质细胞。目前对这类髓样细胞的定义是基于一系列细胞标记物。这些良好的哨兵细胞经历了显著的变化,促进了胶质母细胞瘤的发展,并使其免受治疗。在整个过程中,涉及到大量复杂的机制。人们付出了巨大的努力来破解巨噬细胞/小胶质细胞招募、激活、重编程和功能的神秘代码。我们已经找到了前进的道路。随着越来越多的关键因素被确定,许多新的治疗方法可以被探索,以打破不祥的循环,提高肿瘤对治疗的敏感性,并改善胶质母细胞瘤患者的预后。然而,这可能是一个协同系统,而不是一系列清晰的、逐步的事件。在真理之光能够照亮这个领域之前,仍然存在着重大的挑战。在这里,我们总结了这一领域的最新进展,回顾了我们走过的道路和现在所处的位置。