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UTX constrains antiviral CD8+ T cell responses during chronic virus infection

ABSTRACT: UTX constrains antiviral CD8+ T cell responses during chronic virus infection

PROVIDER: PRJNA601463 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10899684.fastq.gz	Fastqsanger.gz
	SRR10899685.fastq.gz	Fastqsanger.gz
	SRR10899686.fastq.gz	Fastqsanger.gz
	SRR10899687.fastq.gz	Fastqsanger.gz
	SRR10899688.fastq.gz	Fastqsanger.gz

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UTX constrains antiviral CD8+ T cell responses during chronic virus infection

Project description:Persistent virus infections can cause pathogenesis that is debilitating or lethal. During these infections, virus-specific T cells fail to protect due to weakened antiviral activity or failure to persist. These outcomes are governed epigenetically, though it is unknown which enzymes contribute to T cell loss or impaired function over time. Here, we show that T cell receptor-stimulated CD8+ T cells increase their expression of UTX (Ubiquitously transcribed Tetratricopeptide repeat, X-chromosome), an enzyme involved in demethylating histone-3 lysine-27 (H3K27), and reduce genome-wide H3K27-me3. UTX limits the frequency and durability of virus-specific CD8+ T cells during chronic lymphocytic choriomeningitis virus (LCMV) infection in mice by promoting inhibitory receptor expression and apoptosis. UTX also increases effector gene expression to improve CTL-mediated protection, a process corresponding to reduced H3K27me3 at effector gene bodies. Thus, UTX guides gene expression patterns in CD8+ T cells, promoting antiviral activity while reducing CD8+ T cell durability.

2021-02-09 | GSE143736 | GEO

Effect of deletion of UTX expression in NY8.3 progenitor CD8+ T cells

Project description:Type 1 diabetes (T1D) is a chronic autoimmune disease resulting from the destruction of insulin-producing beta cells. This persistence is due to the continual replenishment of short-live effector CD8+ T cells (autoimmune mediators, Tmed) in the pancreatic lymph nodes (pLNs) by a long-lived reservoir of stem-like memory CD8+ T cells (autoimmune progenitors, Tprog). We are investigating an epigenetic regulator UTX playing the role in Tprog to Tmed conversion. The NOD mice with T cell-specific UTX deficiency (UTXTCD mice) were protected from T1D. In addition, the deletion of UTX in CD8+ T cells resulted in the accumulation of Tprog and loss of Tmed populations in pLNs. The function of UTX is to demethylate the histone mark, H3K27 tri-methylation, leading to the open chromatin accessibility for gene expression. ATAC-seq and RNA-seq of antigen specific Tprog cells revealed a role of UTX in closing chromatin at progenitor gene loci while enforcing accessibility at effector gene loci. Taken together, these findings point to the potential of targeting UTX-mediated conversion of Tprog into Tmed for interrupting the T1D autoimmune response.

2024-11-25 | GSE282227 | GEO

Analysis of gene expression sigunature in Utx KO CD8 T cells

Project description:To elucidate the effect of Utx, histone demethylase, on CD8 Tcell diferentiation, The gene expression were measured in WT and Utx KO CD8 T cells.

2023-07-12 | GSE214673 | GEO

Utx interactome in mouse myeloid progenitor cells

Project description:Immunoprecipitation of Utx followed by mass spectrometry analysis to identify Utx binding partners in mouse myeloid progenitor cells.

2018-04-30 | PXD005011 | Pride

T cell UTX promotes Tfh-mediated clearance of persistent virus infection

Project description:Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, promotes the generation of T follicular helper (Tfh) cells, a CD4+ T cell subset essential for B cell antibody generation and clearance of chronic viral infections. Mice with T cell specific UTX deletion (UTX TKO mice) had fewer Tfh cells, showed defective germinal center formation, lacked virus-specific IgG production, and were unable to resolve chronic lymphocytic choriomeningitis virus infection. In UTX TKO T cells, decreased expression of IL-6R±, and other Tfh-related loci, was associated with increased H3K27 methylation. Additionally, Turner Syndrome subjects, who are predisposed to chronic ear infections, have reduced UTX expression in immune cells and decreased Tfh frequency. Thus, we identify a critical link between UTX in T cells and immunity to infection. Mice were infected with chronic LCMV and sorted for Tfh on day 21 pi (sorted for: CD4+CXCR5+CD62Llo T cell). ChIP-Seq and RNA-Seq on WT and Utx KO cells.

2015-09-01 | E-GEOD-64969 | biostudies-arrayexpress

PHD2 constrains the anti-tumor CD8+ T cell activity

Project description:PHD2 constrains the anti-tumor CD8+ T cell activity

| PRJNA894180 | ENA

Alternative mRNA splicing controls functions of the human H3K27 demethylase UTX/KDM6A

Project description:The UTX/KDM6A gene encodes the UTX histone H3K27 demethylase, which plays an important role in mammalian development and is frequently mutated in cancers and particularly, in urothelial cancers. Using BioID technique, we explored the interactome of different UTX isoforms.

2024-01-28 | PXD041254 | Pride

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

Project description:Stem-like CD8 T cells maintain long-term antiviral CD8 immunity during chronic infection, and share regulatory pathways with memory precursor effector cells generated after acute infection. However, it is unclear whether stem-like CD8 T cells require distinct transcriptional and epigenetic regulation for their longevity and adaptation to the immunosuppressive environment in chronic infection. Here, our comparison of single-cell transcriptomes and epigenetic profiles of CD8 T cells responding to acute and chronic viral infections revealed that stem-like CD8 T cells became distinct from memory precursors before clonal expansion ended. We found that a coexpression gene module containing Tox exhibited higher transcriptional activities and active histone marks in stem-like T cells than memory precursors. Moreover, TOX promoted persistence of antiviral CD8 T cells, and was required for stem-like CD8 differentiation. Our results indicate that stem-like CD8 T cells require unique transcriptional and epigenetic programs for their differentiation and persistence during chronic viral infection.

2019-04-16 | GSE119942 | GEO

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

2019-04-16 | GSE119941 | GEO

Longitudinal liver sampling in patients with chronic hepatitis B starting antiviral therapy reveals hepatotoxic CD8+ T cells

Project description:The objective of this study is to identify immunological mechanisms that contribute to normalization of liver inflammation in chronic hepatitis B (CHB) patients starting the antiviral nucleoside analogue, Tenofovir alafenamide (TAF).

2022-12-01 | GSE216314 | GEO

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