The cancer stem cell subtype determines immune infiltration of Glioblastoma

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Output type: Journal article

Author list: Beier C., Kumar P., Meyer K., Leukel P., Bruttel V., Aschenbrenner I., Riemenschneider M., Fragoulis A., Rümmele P., Lamszus K., Schulz J., Weis J., Bogdahn U., Wischhusen J., Hau P., Spang R., Beier D.

Publisher: Mary Ann Liebert

Publication year: 2012

Journal: Stem Cells and Development (1547-3287)

Volume number: 21

Issue number: 15

Start page: 2753

End page: 2761

Number of pages: 9

ISSN: 1547-3287

eISSN: 1557-8534

URL: http://api.elsevier.com/content/abstract/scopus_id:84870439234

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Open access status: green

Full text URL: https://europepmc.org/articles/pmc3464079?pdf=render

Abstract

Immune cell infiltration varies widely between different glioblastomas (GBMs). The underlying mechanism, however, remains unknown. Here we show that TGF-beta regulates proliferation, migration, and tumorigenicity of mesenchymal GBM cancer stem cells (CSCs) in vivo and in vitro. In contrast, proneural GBM CSCs resisted TGF-beta due to TGFR2 deficiency. In vivo, a substantially increased infiltration of immune cells was observed in mesenchymal GBMs, while immune infiltrates were rare in proneural GBMs. On a functional level, proneural CSC lines caused a significantly stronger TGF-beta-dependent suppression of NKG2D expression on CD8 T and NK cells in vitro providing a mechanistic explanation for the reduced immune infiltration of proneural GBMs. Thus, the molecular subtype of CSCs TGF-beta-dependently contributes to the degree of immune infiltration. © Copyright 2012, Mary Ann Liebert, Inc. 2012.

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