Modeling tumor immunity of mouse glioblastoma by exhausted CD8+ T cells

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Modeling tumor immunity of mouse glioblastoma by exhausted CD8+ T cells

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Title: Modeling tumor immunity of mouse glioblastoma by exhausted CD8+ T cells
Author: Nakashima, Hiroshi; Alayo, Quazim A. ORCID  0000-0001-5524-7105 ; Penaloza-MacMaster, Pablo; Freeman, Gordon J.; Kuchroo, Vijay K.; Reardon, David A.; Fernandez, Soledad; Caligiuri, Michael; Chiocca, E. Antonio

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Citation: Nakashima, Hiroshi, Quazim A. Alayo, Pablo Penaloza-MacMaster, Gordon J. Freeman, Vijay K. Kuchroo, David A. Reardon, Soledad Fernandez, Michael Caligiuri, and E. Antonio Chiocca. 2018. “Modeling tumor immunity of mouse glioblastoma by exhausted CD8+ T cells.” Scientific Reports 8 (1): 208. doi:10.1038/s41598-017-18540-2. http://dx.doi.org/10.1038/s41598-017-18540-2.
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Abstract: T cell exhaustion occurs during chronic infection and cancers. Programmed cell death protein-1 (PD-1) is a major inhibitory checkpoint receptor involved in T cell exhaustion. Blocking antibodies (Abs) against PD-1 or its ligand, PD-L1, have been shown to reverse T cell exhaustion during chronic infection and cancers, leading to improved control of persistent antigen. However, modeling tumor-specific T cell responses in mouse has been difficult due to the lack of reagents to detect and phenotype tumor-specific immune responses. We developed a novel mouse glioma model expressing a viral epitope derived from lymphocytic choriomeningitis virus (LCMV), which allowed monitoring of tumor-specific CD8 T-cell responses. These CD8 T cells express high levels of PD-1 and are unable to reject tumors, but this can be reversed by anti-PD-1 treatment. These results suggest the efficacy of PD-1 blockade as a treatment for glioblastoma, an aggressive tumor that results in a uniformly lethal outcome. Importantly, this new syngeneic tumor model may also provide further opportunities to characterize anti-tumor T cell exhaustion and develop novel cancer immunotherapies.
Published Version: doi:10.1038/s41598-017-18540-2
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5760520/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:34869008
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