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Cdk5 disruption attenuates tumor PD-L1 expression and promotes antitumor immunity
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Cdk5 disruption attenuates tumor PD-L1 expression and promotes antitumor immunity
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Cdk5 disruption attenuates tumor PD-L1 expression and promotes antitumor immunity
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Journal Article
Cdk5 disruption attenuates tumor PD-L1 expression and promotes antitumor immunity
2016
Overview
Cancers often evade immune surveillance by adopting peripheral tissue- tolerance mechanisms, such as the expression of programmed cell death ligand 1 (PD-L1), the inhibition of which results in potent antitumor immunity. Here, we show that cyclin-dependent kinase 5 (Cdk5), a serine-threonine kinase that is highly active in postmitotic neurons and in many cancers, allows medulloblastoma (MB) to evade immune elimination. Interferon-γ (IFN-γ)-induced PD-L1 up-regulation on MB requires Cdk5, and disruption of Cdk5 expression in a mouse model of MB results in potent CD4(+) T cell-mediated tumor rejection. Loss of Cdk5 results in persistent expression of the PD-L1 transcriptional repressors, the interferon regulatory factors IRF2 and IRF2BP2, which likely leads to reduced PD-L1 expression on tumors. Our finding highlights a central role for Cdk5 in immune checkpoint regulation by tumor cells.
Publisher
The American Association for the Advancement of Science
Subject
/ Cancer
/ CD4-Positive T-Lymphocytes - immunology
/ Cerebellar Neoplasms - genetics
/ Cerebellar Neoplasms - immunology
/ Cyclin-Dependent Kinase 5 - genetics
/ Cyclin-Dependent Kinase 5 - physiology
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Immunity
/ Interferon Regulatory Factor-2 - genetics
/ Interferon Regulatory Factor-2 - metabolism
/ Kinases
/ Male
/ Medulloblastoma - immunology
/ Mice
/ Neoplasms, Experimental - genetics
/ Neoplasms, Experimental - immunology
/ Neurons
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Tumors
