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Data from Glioma-Associated Cytomegalovirus Mediates Subversion of the Monocyte Lineage to a Tumor Propagating Phenotype
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Data from Glioma-Associated Cytomegalovirus Mediates Subversion of the Monocyte Lineage to a Tumor Propagating Phenotype
Data from Glioma-Associated Cytomegalovirus Mediates Subversion of the Monocyte Lineage to a Tumor Propagating Phenotype
KD
Kristine Dziurzynski
Kristine Dziurzynski
JW
Jun Wei
Jun Wei
WQ
Wei Qiao
Wei Qiao
MH
Mustafa Aziz Hatiboglu
Mustafa Aziz Hatiboglu
LK
Ling-Yuan Kong
Ling-Yuan Kong
AW
Adam Wu
Adam Wu
YW
Yongtao Wang
Yongtao Wang
DC
Daniel Cahill
Daniel Cahill
NL
Nicholas Levine
Nicholas Levine
SP
Sujit Prabhu
Sujit Prabhu
GR
Ganesh Rao
Ganesh Rao
RS
Raymond Sawaya
Raymond Sawaya
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31 March 2023
other
Published by
American Association for Cancer Research (AACR)
https://doi.org/10.1158/1078-0432.c.6519516
Abstract
Purpose: Cytomegalovirus (CMV) has been ubiquitously detected within high-grade gliomas, but its role in gliomagenesis has not been fully elicited.Experimental Design: Glioblastoma multiforme (GBM) tumors were analyzed by flow cytometry to determine CMV antigen expression within various glioma-associated immune populations. The glioma cancer stem cell (gCSC) CMV interleukin (IL)-10 production was determined by ELISA. Human monocytes were stimulated with recombinant CMV IL-10 and levels of expression of p-STAT3, VEGF (vascular endothelial growth factor), TGF-β, viral IE1, and pp65 were determined by flow cytometry. The influence of CMV IL-10–treated monocytes on gCSC biology was ascertained by functional assays.Results: CMV showed a tropism for macrophages (MΦ)/microglia and CD133+ gCSCs within GBMs. The gCSCs produce CMV IL-10, which induces human monocytes (the precursor to the central nervous system MΦs/microglia) to assume an M2 immunosuppressive phenotype (as manifested by downmodulation of the major histocompatibility complex and costimulatory molecules) while upregulating immunoinhibitory B7-H1. CMV IL-10 also induces expression of viral IE1, a modulator of viral replication and transcription in the monocytes. Finally, the CMV IL-10–treated monocytes produced angiogenic VEGF, immunosuppressive TGF-β, and enhanced migration of gCSCs.Conclusions: CMV triggers a feedforward mechanism of gliomagenesis by inducing tumor-supportive monocytes. Clin Cancer Res; 17(14); 4642–9. ©2011 AACR.
Keywords
VIRAL REPLICATION
MONOCYTES
ANTIGEN
CMV
TUMORS
FUNCTIONAL
GCSC
GLIOMA
CANCER
HISTOCOMPATIBILITY COMPLEX
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