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

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

PROVIDER: PRJNA1050148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27144200_1.fastq.gz	Fastqsanger.gz
	SRR27144200_2.fastq.gz	Fastqsanger.gz
	SRR27144201_1.fastq.gz	Fastqsanger.gz
	SRR27144201_2.fastq.gz	Fastqsanger.gz
	SRR27144202_1.fastq.gz	Fastqsanger.gz

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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

| PRJNA1050145 | ENA

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 [ChIP-seq]

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

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

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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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Project description:Nuclear receptor subfamily 2, group F, member 6 (NR2F6) is an orphan member of the nuclear receptor superfamily. Here, we show that genetic ablation of Nr2f6 significantly improves survival in the murine transgenic TRAMP prostate cancer model. Furthermore, Nr2f6(-/-) mice spontaneously reject implanted tumors and develop host-protective immunological memory against tumor rechallenge. This is paralleled by increased frequencies of both CD4(+) and CD8(+) T cells and higher expression levels of interleukin 2 and interferon ? at the tumor site. Mechanistically, CD4(+) and CD8(+) T cell-intrinsic NR2F6 acts as a direct repressor of the NFAT/AP-1 complex on both the interleukin 2 and the interferon ? cytokine promoters, attenuating their transcriptional thresholds. Adoptive transfer of Nr2f6-deficient T cells into tumor-bearing immunocompetent mice is sufficient to delay tumor outgrowth. Altogether, this defines NR2F6 as an intracellular immune checkpoint in effector T cells, governing the amplitude of anti-cancer immunity.

| S-EPMC4594157 | biostudies-literature

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