TIGIT and PD-1 Immune Checkpoint Pathways Are Associated With Patient Outcome and Anti-Tumor Immunity in Glioblastoma.
Animals
B7-H1 Antigen
/ antagonists & inhibitors
Brain Neoplasms
/ immunology
CD8-Positive T-Lymphocytes
/ immunology
Cell Line, Tumor
Cell Proliferation
/ drug effects
Glioblastoma
/ immunology
Humans
Immune Checkpoint Inhibitors
/ pharmacology
Immune Checkpoint Proteins
/ metabolism
Immunotherapy
/ methods
Lymphocytes, Tumor-Infiltrating
/ metabolism
Mice
Mice, Inbred C57BL
Myeloid-Derived Suppressor Cells
/ drug effects
Programmed Cell Death 1 Receptor
/ antagonists & inhibitors
Receptors, Immunologic
/ antagonists & inhibitors
Tumor Microenvironment
/ drug effects
MDSCs
PD1
TIGIT
gene network analyses
glioblastoma
immunotherapy
myeloid suppressor cell
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
02
12
2020
accepted:
12
04
2021
entrez:
24
5
2021
pubmed:
25
5
2021
medline:
24
9
2021
Statut:
epublish
Résumé
Glioblastoma (GBM) remains an aggressive brain tumor with a high rate of mortality. Immune checkpoint (IC) molecules are expressed on tumor infiltrating lymphocytes (TILs) and promote T cell exhaustion upon binding to IC ligands expressed by the tumor cells. Interfering with IC pathways with immunotherapy has promoted reactivation of anti-tumor immunity and led to success in several malignancies. However, IC inhibitors have achieved limited success in GBM patients, suggesting that other checkpoint molecules may be involved with suppressing TIL responses. Numerous IC pathways have been described, with current testing of inhibitors underway in multiple clinical trials. Identification of the most promising checkpoint pathways may be useful to guide the future trials for GBM. Here, we analyzed the The Cancer Genome Atlas (TCGA) transcriptomic database and identified PD1 and TIGIT as top putative targets for GBM immunotherapy. Additionally, dual blockade of PD1 and TIGIT improved survival and augmented CD8
Identifiants
pubmed: 34025646
doi: 10.3389/fimmu.2021.637146
pmc: PMC8137816
doi:
Substances chimiques
B7-H1 Antigen
0
CD274 protein, human
0
Immune Checkpoint Inhibitors
0
Immune Checkpoint Proteins
0
PDCD1 protein, human
0
Programmed Cell Death 1 Receptor
0
Receptors, Immunologic
0
TIGIT protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
637146Subventions
Organisme : NCI NIH HHS
ID : R01 CA244520
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA222804
Pays : United States
Informations de copyright
Copyright © 2021 Raphael, Kumar, McCarl, Shoger, Wang, Sandlesh, Sneiderman, Allen, Zhai, Campagna, Foster, Bruno, Agnihotri, Hu, Castro, Lieberman, Broniscer, Diaz, Amankulor, Rajasundaram, Pollack and Kohanbash.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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