Department of Fundamental and Applied Neurobiology, V. P. Serbsky National Medical Research Center of Psychiatry and Narcology, The Ministry of Health of the Russian Federation, Moscow, Russia.
Department of Medical Nanobiotechnology, Institute of Translational Medicine, N.I. Pirogov Russian National Research Medical University, The Ministry of Health of the Russian Federation, Moscow, Russia.
Front Immunol. 2024 Feb 8;15:1326757. doi: 10.3389/fimmu.2024.1326757. eCollection 2024.
Despite significant advances in our knowledge regarding the genetics and molecular biology of gliomas over the past two decades and hundreds of clinical trials, no effective therapeutic approach has been identified for adult patients with newly diagnosed glioblastoma, and overall survival remains dismal. Great hopes are now placed on combination immunotherapy. In clinical trials, immunotherapeutics are generally tested after standard therapy (radiation, temozolomide, and steroid dexamethasone) or concurrently with temozolomide and/or steroids. Only a minor subset of patients with progressive/recurrent glioblastoma have benefited from immunotherapies. In this review, we comprehensively discuss standard therapy-related systemic immunosuppression and lymphopenia, their prognostic significance, and the implications for immunotherapy/oncolytic virotherapy. The effectiveness of immunotherapy and oncolytic virotherapy (viro-immunotherapy) critically depends on the activity of the host immune cells. The absolute counts, ratios, and functional states of different circulating and tumor-infiltrating immune cell subsets determine the net immune fitness of patients with cancer and may have various effects on tumor progression, therapeutic response, and survival outcomes. Although different immunosuppressive mechanisms operate in patients with glioblastoma/gliomas at presentation, the immunological competence of patients may be significantly compromised by standard therapy, exacerbating tumor-related systemic immunosuppression. Standard therapy affects diverse immune cell subsets, including dendritic, CD4+, CD8+, natural killer (NK), NKT, macrophage, neutrophil, and myeloid-derived suppressor cell (MDSC). Systemic immunosuppression and lymphopenia limit the immune system's ability to target glioblastoma. Changes in the standard therapy are required to increase the success of immunotherapies. Steroid use, high neutrophil-to-lymphocyte ratio (NLR), and low post-treatment total lymphocyte count (TLC) are significant prognostic factors for shorter survival in patients with glioblastoma in retrospective studies; however, these clinically relevant variables are rarely reported and correlated with response and survival in immunotherapy studies (e.g., immune checkpoint inhibitors, vaccines, and oncolytic viruses). Our analysis should help in the development of a more rational clinical trial design and decision-making regarding the treatment to potentially improve the efficacy of immunotherapy or oncolytic virotherapy.
尽管在过去的二十年中,我们在神经胶质瘤的遗传学和分子生物学方面取得了重大进展,并且进行了数百项临床试验,但仍未找到新诊断为胶质母细胞瘤的成年患者的有效治疗方法,总体生存率仍然很低。目前人们对联合免疫疗法寄予厚望。在临床试验中,免疫疗法通常在标准治疗(放疗、替莫唑胺和类固醇地塞米松)后或与替莫唑胺和/或类固醇同时进行测试。只有一小部分进展/复发性胶质母细胞瘤患者从免疫治疗中受益。在这篇综述中,我们全面讨论了与标准治疗相关的系统性免疫抑制和淋巴细胞减少症,及其预后意义,以及对免疫治疗/溶瘤病毒治疗的影响。免疫治疗和溶瘤病毒治疗(病毒免疫治疗)的有效性取决于宿主免疫细胞的活性。不同循环和肿瘤浸润免疫细胞亚群的绝对计数、比例和功能状态决定了癌症患者的净免疫适应性,并可能对肿瘤进展、治疗反应和生存结果产生各种影响。尽管在出现胶质母细胞瘤/神经胶质瘤时不同的免疫抑制机制在患者中起作用,但标准治疗可能会显著损害患者的免疫能力,从而加剧与肿瘤相关的系统性免疫抑制。标准治疗会影响多种免疫细胞亚群,包括树突状细胞、CD4+、CD8+、自然杀伤(NK)、NKT、巨噬细胞、中性粒细胞和髓系来源的抑制细胞(MDSC)。系统性免疫抑制和淋巴细胞减少限制了免疫系统靶向胶质母细胞瘤的能力。需要改变标准治疗以提高免疫治疗的成功率。在回顾性研究中,类固醇的使用、高中性粒细胞与淋巴细胞比值(NLR)和低治疗后总淋巴细胞计数(TLC)是胶质母细胞瘤患者生存时间更短的显著预后因素;然而,这些具有临床意义的变量很少被报道,并且与免疫治疗研究中的反应和生存相关(例如,免疫检查点抑制剂、疫苗和溶瘤病毒)。我们的分析应该有助于制定更合理的临床试验设计和治疗决策,从而有可能提高免疫治疗或溶瘤病毒治疗的疗效。