Abstract
Recent studies demonstrated that CD155 plays an important role in anti-tumor immune responses. However, its role in glioma remains unclear. Here, we identify CD155 as a promising immune target in glioma. CD155 expression was significantly highly expressed in glioblastoma but not in normal brain tissue. Subsequent analysis based on genetic and clinical data from 1173 glioma patients in Rembrandt and TCGA dataset suggested that CD155 related genes of immune response were mainly positively correlated with CD155 expression. CD155 expression was positively correlated with immune-related metagenes STAT1, HCK, LCK, and MHC I but negatively associated with IgG. CD155 expression was positively correlated with biomarker gene expression of infiltrating immune cells, suggested that high CD155 expression in gliomas tend to have more infiltrating immune cells compared with gliomas with low CD155 expression. Pearson correlation analysis showed that CD155 is associated with CD96, CD226, Nectin4, PD-L1, B7-H2, NR2F6 and GITR, implying the potential synergistic effects of these checkpoint proteins. These findings implied that CD155 is a promising immunotherapy target, combined with existing immune checkpoint blockade therapies for glioma.
Highlights
Glioma, especially high-grade glioma (HGG) is a severe malignant brain tumor associated with an extremely aggressive clinical course and poor overall survival (OS)
Recent studies demonstrated that CD155 plays an important role in anti-tumor immune responses [9]
Hepatocellular carcinoma patients with up-regulated CD155 expression within tumor are strongly associated with worse prognosis, the presence of anti-CD155 antibody can significantly increases lysis of hepatoma cell line HepG2 by natural killer (NK) cells [24]
Summary
Especially high-grade glioma (HGG) is a severe malignant brain tumor associated with an extremely aggressive clinical course and poor overall survival (OS). Recent years have been associated with striking success in tumor immunotherapy, especially checkpoint inhibitors that target programmed cell death protein 1 (PD-1) / programmed death ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) [6]. Whereas several studies on checkpoint inhibitors have been exploited and applied to clinical settings for gliomas, many patients do not respond to these therapies [6, 7]. This has catalyzed enormous interest in the identification of additional targets to increase response rates and improve therapeutic efficacy
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
