目前的治疗策略在治疗胶质母细胞瘤（成人最常见的原发性脑肿瘤）方面仍然只取得了有限的成功。除了肿瘤微环境的特征之外，还描述了胶质母细胞瘤患者大脑的整体变化。然而，原发肿瘤部位远处神经炎症的影响和分子特征尚未完全阐明。我们对新诊断的胶质母细胞瘤 (n=41)、WHO 2 级星形细胞瘤 (n= 7) 和健康对照 (n=20) 并比较非病变（即对侧）半球的 TSPO-PET 信号。使用同源 SB28 胶质母细胞瘤小鼠的回译来表征细胞水平上的 PET 改变。最终，多重基因表达分析用于分析远程大脑中的免疫细胞。我们的研究显示，与健康对照相比，新诊断的胶质母细胞瘤患者对侧半球的 TSPO-PET 信号升高。对侧 TSPO 与持续癫痫发作和较短的总生存期相关，与肿瘤表型无关。对同基因胶质母细胞瘤小鼠的反向翻译确定了骨髓细胞是对侧 TSPO-PET 信号增加的主要来源，并确定了一种复杂的免疫特征，其特征是远处大脑区域的骨髓细胞激活和免疫抑制。可以用 TSPO- 检测对侧半球内的神经炎症。 PET 成像与新诊断的胶质母细胞瘤患者的不良预后相关。远程神经炎症的分子特征促进了对有害全脑炎症患者的免疫调节策略的评估，如高 TSPO 表达所反映的那样。

Current therapy strategies still provide only limited success in the treatment of glioblastoma, the most frequent primary brain tumor in adults. In addition to the characterization of the tumor microenvironment, global changes in brain of patients with glioblastoma have been described. However, the impact and molecular signature of neuroinflammation distant of the primary tumor site have not yet been thoroughly elucidated.We performed translocator protein (TSPO)-PET in patients with newly diagnosed glioblastoma (n=41), astrocytoma WHO grade 2 (n=7) and healthy controls (n=20) and compared TSPO-PET signals of the non-lesion (i.e. contralateral) hemisphere. Back-translation in syngeneic SB28 glioblastoma mice was used to characterize PET alterations on a cellular level. Ultimately, multiplex gene expression analyses served to profile immune cells in remote brain.Our study revealed elevated TSPO-PET signals in contralateral hemispheres of patients with newly diagnosed glioblastoma compared to healthy controls. Contralateral TSPO was associated with persisting epileptic seizures and shorter overall survival independent of the tumor phenotype. Back-translation into syngeneic glioblastoma mice pinpointed myeloid cells as the predominant source of contralateral TSPO-PET signal increases and identified a complex immune signature characterized by myeloid cell activation and immunosuppression in distant brain regions.Neuroinflammation within the contralateral hemisphere can be detected with TSPO-PET imaging and associates with poor outcome in patients with newly diagnosed glioblastoma. The molecular signature of remote neuroinflammation promotes the evaluation of immunomodulatory strategies in patients with detrimental whole brain inflammation as reflected by high TSPO expression.