刺
溶瘤病毒
癌症研究
胶质瘤
免疫系统
肿瘤微环境
免疫疗法
信号转导
干扰素基因刺激剂
医学
免疫检查点
生物
免疫学
先天免疫系统
细胞生物学
航空航天工程
工程类
作者
Justin Low,Michael C. Brown,Zachary J. Reitman,Joshua D. Bernstock,James M. Markert,Gregory K. Friedman,Matthew S. Waitkus,Michelle Bowie,David M. Ashley
摘要
Since the discovery that cGAS/STING recognizes endogenous DNA released from dying cancer cells and induces type I interferon and antitumor T cell responses, efforts to understand and therapeutically target the STING pathway in cancer have ensued. Relative to other cancer types, the glioma immune microenvironment harbors few infiltrating T cells, but abundant tumor-associated myeloid cells, possibly explaining disappointing responses to immune checkpoint blockade therapies in cohorts of patients with glioblastoma. Notably, unlike most extracranial tumors, STING expression is absent in the malignant compartment of gliomas, likely due to methylation of the STING promoter. Nonetheless, several preclinical studies suggest that inducing cGAS/STING signaling in the glioma immune microenvironment could be therapeutically beneficial, and cGAS/STING signaling has been shown to mediate inflammatory and antitumor effects of other modalities either in use or being developed for glioblastoma therapy, including radiation, tumor-treating fields, and oncolytic virotherapy. In this Review, we discuss cGAS/STING signaling in gliomas, its implications for glioma immunobiology, compartment-specific roles for STING signaling in influencing immune surveillance, and efforts to target STING signaling - either directly or indirectly - for antiglioma therapy.
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