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. 2022 Aug 16;13:4814. doi: 10.1038/s41467-022-32430-w

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 9 — Collectively, data suggests a model in which EGFR activation (adult IDH-WT glioblastoma), PDGFRA activation (pediatric high-grade glioma) and/or hypoxia promote CD73 expression by tumor cells in an inflammatory microenvironment. Spatial co-localization of tumor cell-specific CD73 with microglial CD39 augments adenosine production in the tumor microenvironment, promoting immune tolerance and tumorigenesis through action on multiple cell populations. Created with BioRender.com.