Ezh2 phosphorylation state determines its capacity to maintain CD8+ T memory precursors for antitumor immunity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Shan He, Yongnian Liu, Lijun Meng, Hongxing Sun, Ying Wang, Yun Ji, Janaki Purushe, Pan Chen, Changhong Li, Jozef Madzo, Jean-Pierre Issa, Jonathan Soboloff, Ran Reshef, Bethany Moore, Luca Gattinoni, Yi Zhang

ABSTRACT

Memory T cells sustain effector T-cell production while self-renewing in reaction to persistent antigen; yet, excessive expansion reduces memory potential and impairs antitumor immunity. Epigenetic mechanisms are thought to be important for balancing effector and memory differentiation; however, the epigenetic regulator(s) underpinning this process remains unknown. Herein, we show that the histone methyltransferase Ezh2 controls CD8+ T memory precursor formation and antitumor activity. Ezh2 activates Id3 while silencing Id2, Prdm1 and Eomes, promoting the expansion of memory precursor cells and their differentiation into functional memory cells. Akt activation phosphorylates Ezh2 and decreases its control of these transcriptional programs, causing enhanced effector differentiation at the expense of T memory precursors. Engineering T cells with an Akt-insensitive Ezh2 mutant markedly improves their memory potential and capability of controlling tumor growth compared to transiently inhibiting Akt. These findings establish Akt-mediated phosphorylation of Ezh2 as a critical target to potentiate antitumor immunotherapeutic strategies. More... »

PAGES

2125

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-017-02187-8

    DOI

    http://dx.doi.org/10.1038/s41467-017-02187-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1099598270

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29242551


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