尽管常规疗法在治疗儿童脑瘤（PBTs）方面的生存率进展不大，不能完全治愈，但迫切需要新的策略来克服传统疗法的毒副作用。共抑制免疫检查点分子（如CTLA-4、PD-1/PD-L1等）和组蛋白变种中的表观遗传改变（例如在肿瘤微环境中帮助免疫逃逸的H3K27me3）在PBTs的治疗中并没有引起太多关注。然而，对组蛋白蛋白中的乙酰化、甲基化、磷酸化、泛素化、泛素乙酰化和泛素类多聚（ADP）核糖化等关键表观遗传机制性改变已经得到广泛认可。儿童脑瘤中的关键检查点包括细胞毒性T淋巴细胞抗原-4（CTLA-4）、程序性细胞死亡蛋白-1（PD-1）、程序性死亡配体-1（PDL1）、OX-2膜糖蛋白（CD200）和吲哚胺2,3-二氧化酶（IDO）。本综述文章涵盖了多种共抑制免疫检查点蛋白和组蛋白表观遗传改变在不同癌症中的作用的现状。我们进一步讨论了这些检查点背后的机制、细胞信号传导、临床和临床前研究的现状以及儿童脑瘤免疫治疗的未来机会。总之，本文进一步讨论了这些干预措施在提供更好疗法选择方面的可能性。版权所有© Bentham Science Publishers；如有任何疑问，请发送电子邮件至 epub@benthamscience.net。

Despite little progress in survival rates with regular therapies, which do not provide complete care for curing pediatric brain tumors (PBTs), there is an urgent need for novel strategies to overcome the toxic effects of conventional therapies to treat PBTs. The co-inhibitory immune checkpoint molecules, e.g., CTLA-4, PD-1/PD-L1, etc., and epigenetic alterations in histone variants, e.g., H3K27me3 that help in immune evasion at tumor microenvironment have not gained much attention in PBTs treatment. However, key epigenetic mechanistic alterations, such as acetylation, methylation, phosphorylation, sumoylation, poly (ADP)-ribosylation, and ubiquitination in histone protein, are greatly acknowledged. The crucial checkpoints in pediatric brain tumors are cytotoxic T lymphocyte antigen-4 (CTLA-4), programmed cell death protein-1 (PD-1) and programmed death-ligand 1 (PDL1), OX-2 membrane glycoprotein (CD200), and indoleamine 2,3-dioxygenase (IDO). This review covers the state of knowledge on the role of multiple co-inhibitory immunological checkpoint proteins and histone epigenetic alterations in different cancers. We further discuss the processes behind these checkpoints, cell signalling, the current scenario of clinical and preclinical research and potential futuristic opportunities for immunotherapies in the treatment of pediatric brain tumors. Conclusively, this article further discusses the possibilities of these interventions to be used for better therapy options.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.