Literature DB >> 21490182

Glioma-associated cytomegalovirus mediates subversion of the monocyte lineage to a tumor propagating phenotype.

Kristine Dziurzynski1, Jun Wei, Wei Qiao, Mustafa Aziz Hatiboglu, Ling-Yuan Kong, Adam Wu, Yongtao Wang, Daniel Cahill, Nicholas Levine, Sujit Prabhu, Ganesh Rao, Raymond Sawaya, Amy B Heimberger.   

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.

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Year:  2011        PMID: 21490182      PMCID: PMC3139801          DOI: 10.1158/1078-0432.CCR-11-0414

Source DB:  PubMed          Journal:  Clin Cancer Res        ISSN: 1078-0432            Impact factor:   12.531


  47 in total

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