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Nuclear Receptor NR2F6 as an Alternative Cancer Immune Checkpoint in the T Cell Compartment

ABSTRACT: Nuclear Receptor NR2F6 as an Alternative Cancer Immune Checkpoint in the T Cell Compartment

OTHER RELATED OMICS DATASETS IN: GSE111796

PROVIDER: PRJNA438152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6830300.fastq.gz	Fastqsanger.gz
	SRR6830310.fastq.gz	Fastqsanger.gz
	SRR6830301.fastq.gz	Fastqsanger.gz
	SRR6830311.fastq.gz	Fastqsanger.gz
	SRR6830302.fastq.gz	Fastqsanger.gz

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Nuclear Receptor NR2F6 as an Alternative Cancer Immune Checkpoint in the T Cell Compartment

Project description:Analyzing mouse tumor models in vivo, human T cells ex vivo and human lung cancer samples, we provide direct evidence that NR2F6 acts as novel immune checkpoint. Genetic ablation of Nr2f6, particularly in combination with blockade of the established PD-L1 cancer immune checkpoint, efficiently delayed tumor progression and improved survival in experimental mouse models. The target genes deregulated in intratumoral T lymphocytes upon genetic ablation of Nr2f6 alone or together with PD-L1 blockade, revealed multiple advantageous transcriptional alterations for effective tumor rejection. In keeping with the above observation, acute Nr2f6 silencing in both mouse and human T cells induced hyper-responsiveness that established a non-redundant T cell-inhibitory function of NR2F6. Analyzing mouse tumor models in vivo, human T cells ex vivo and human lung cancer samples,

2018-03-14 | GSE111796 | GEO

Melanoma-intrinsic NR2F6 activity regulates anti-tumor immunity

Project description:Nuclear receptors (NRs) are implicated in the regulation of tumors and immune cells. We identify a tumor-intrinsic function of the orphan NR, NR2F6, regulating anti-tumor immunity. NR2F6 was selected from 48 candidate NRs, based on an expression pattern in melanoma patient specimens (i.e., IFN signature) associated with positive responses to immunotherapy and favorable patient outcomes. Correspondingly, genetic ablation of NR2F6 in a mouse melanoma model conferred a more effective response to PD-1 therapy. NR2F6 loss in B16F10 and YUMM1.7 melanoma cells attenuated tumor development in immune-competent but not -incompetent mice via the increased abundance of effector and progenitor-exhausted CD8+ T cells. Inhibition of NACC1 and FKBP10, identified as NR2F6 effectors, phenocopied NR2F6 loss. Remarkably, inoculation of NR2F6 KO mice with NR2F6 KD melanoma cells further decreased tumor growth compared with NR2F6 WT mice. Tumor-intrinsic NR2F6 function complements its tumor-extrinsic role and justifies the development of novel anti-cancer therapies.

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The roles of nuclear orphan receptor NR2F6 in anti-viral innate immunity [RNA-seq]

Project description:The regulation of proper gene transcription is critical for anti-viral defense. Dynamics of enhancer activity play important roles in many biological processes, and epigenomic analysis is widely used to determine the involved enhancers and transcription factors. To determine new transcription factors in anti-DNA-virus response, we perform H3K27ac ChIP-Seq analysis to profile the active enhancer pattern in HSV-1-infected THP-1 cells. We have identified three transcription factors, NR2F6, MEF2D and MAFF, and experimentally verified their roles in promoting HSV-1 replication. NR2F6 promotes HSV-1 replication and gene expression in vitro and in vivo, which is not related with the classical cGAS/STING pathway. NR2F6 binds to the promoter of MAP3K5 and activate AP-1/c-Jun pathway, which is critical for DNA virus replication. On the contrary, NR2F6 expression is transcriptionally repressed by c-Jun upon HSV-1 infection, which forms a negative feedback loop. Meanwhile, cGAS/STING innate immunity signaling represses NR2F6 through STAT3. Taken together, we have identified new transcription factors involved in the interactive network between DNA viruses and host cells, and revealed the underlying mechanisms for anti-viral research.

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The roles of nuclear orphan receptor NR2F6 in anti-viral innate immunity

Project description:The roles of nuclear orphan receptor NR2F6 in anti-viral innate immunity

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The roles of nuclear orphan receptor NR2F6 in anti-viral innate immunity [ChIP-seq]

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The replication checkpoint protects fork stability by releasing transcribed genes from nuclear pores.

Project description:Transcription hinders replication fork progression and stability, and the Mec1/ATR checkpoint protects fork integrity. Examining checkpoint-dependent mechanisms controlling fork stability, we find that fork reversal or dormant origin firing owing to checkpoint defects are rescued in checkpoint mutants lacking THO, TREX-2 or inner basket nucleoporins. Gene gating tethers transcribed genes to the nuclear periphery and is counteracted by checkpoint kinases through phosphorylation of nucleoporins such as Mlp1. Checkpoint mutants fail to detach transcribed genes from nuclear pores, thus generating topological impediments for incoming forks. Releasing this topological complexity by introducing a double-strand break between a fork and a transcribed unit prevents fork collapse. Mlp1 mutants mimicking constitutive checkpoint-dependent phosphorylation also alleviate checkpoint defects. We propose that the checkpoint assists fork progression and stability at transcribed genes by phosphorylating key nucleoporins and counteracting gene gating, thus neutralizing the topological tension generated at nuclear pore gated genes.

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