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. 2021 Feb 28;14(3):200. doi: 10.3390/ph14030200

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Mechanisms of CD226 downregulation. (Left) Tumor microenvironment promotes the accumulation of a subset of CD8⁺ T cells that lose CD226. CD226 is transcriptionally downregulated in an eomesodermin (Eomes)-dependent and a PVR-independent manner. CD226 downregulation is abolished in Eomes-deficient CD8⁺ T cells. Eomes directly interacts with regulatory elements of the CD226 gene. (Right) CD226 expression is posttranslationally regulated through the ubiquitin–proteasome pathway. After engagement with PVR, mouse CD226 is phosphorylated at Y319 by Scr kinase, subsequently recruiting E3 ubiquitin ligase Cbl-b, which induces ubiquitination-dependent proteasomal degradation of phosphorylated CD226.