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Loss of PBAF Promotes Effector Differentiation and Limits CD8+ T Cell Exhaustion in Chronic Viral Infection and Cancer [multiomics]

ABSTRACT: Loss of PBAF Promotes Effector Differentiation and Limits CD8+ T Cell Exhaustion in Chronic Viral Infection and Cancer [multiomics]

PROVIDER: PRJNA919061 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23000437_1.fastq.gz	Fastqsanger.gz
	SRR23000437_2.fastq.gz	Fastqsanger.gz
	SRR23000438_1.fastq.gz	Fastqsanger.gz
	SRR23000438_2.fastq.gz	Fastqsanger.gz
	SRR23000439_1.fastq.gz	Fastqsanger.gz

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Loss of PBAF Promotes Effector Differentiation and Limits CD8+ T Cell Exhaustion in Chronic Viral Infection and Cancer

Project description:Loss of PBAF Promotes Effector Differentiation and Limits CD8+ T Cell Exhaustion in Chronic Viral Infection and Cancer

| PRJNA919053 | ENA

Loss of PBAF Promotes Effector Differentiation and Limits CD8+ T Cell Exhaustion in Chronic Viral Infection and Cancer [multiomics]

Project description:To gain insights into how PBAF complex regulates dynamic chromatin structure changes in LCMV-specific CD8+ T cells during chronic viral infection and examine the how PBAF-deficiency alters the transcriptional and epigenetic heterogeneity of CD8+ T cells, we performed single cell RNA + ATAC multiomic sequencing on Arid2- and Pbrm1-deficient CD8+ T cells and their wild-type counterpart.

2023-06-22 | GSE222346 | GEO

Transcriptome differences in HCC infiltrated CD8+ T cells in effector and exhaustion state

Project description:CD8+ T cells isolated from HCC tissue were divided into three groups: PD1-TIM3- CD8+ TILs, exhibiting full effector function; PD1-intTIM3+ CD8+ TILs, exhibiting partial exhaustion; and PD1-hiTIM3+ CD8+ TILs, exhibiting severe exhaustion, as reflected by the differences in their ability to produce effector cytokines respectively. Transcriptome sequence analysis was performed to investigate the gene expression profile was performed.

2019-12-31 | E-MTAB-7278 | biostudies-arrayexpress

Screening for ceramide effector molecules using multiomics approaches

Project description:Screening for ceramide effector molecules using multiomics approaches

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MARCH1 controls an exhaustion-like program of effector CD4+ T cells promoting allergic airway inflammation

Project description:Persistent antigenic signalling leads to T cell exhaustion, a dysfunctional state arising in many chronic infections and cancers. Little is known concerning mechanisms limiting exhaustion in immune stimulatory diseases such as asthma. We report that membrane-associated RING-CH1 (MARCH1), the ubiquitin ligase that mediates surface turnover of MHCII and CD86 in professional APCs, plays an essential role in restraining exhaustion of effector CD4+ T cells in a mouse model of asthma. Mice lacking MARCH1 or the ubiquitin acceptor sites of MHCII and CD86 exhibited increased MHCII and CD86 surface expression on lung APCs, and this increase promoted enhanced expression of immune inhibitory receptors by effector CD4+ T cells and inhibited their proliferation. Remarkably, ablation of MARCH1 in mice with established asthma reduced airway infiltration of eosinophils and Th2 cells. Thus, MARCH1 controls exhaustion of effector CD4+ T cells during allergic airway inflammation and may serve as a therapeutic target for asthma.

2022-08-24 | GSE211511 | GEO

Direct regulation of T cell exhaustion by NFAT [RNA-Seq]

Project description:During persistent antigen stimulation, CD8+ cytolytic T cells (CTL) show a gradual decrease in effector function, or “exhaustion”, which impairs the immune response to tumors and infections. Here we show that NFAT, a transcription factor with an established role in T cell activation, in parallel controls a second transcriptional program conferring the characteristic features of CD8+ T cell exhaustion, including upregulation of genes encoding inhibitory cell surface receptors and diminished TCR signaling. Expression of an engineered NFAT1, which induces this negative regulatory program in the absence of the effector program, interferes with the ability of CD8+ T cells to protect against Listeria infection or attenuate tumor growth in vivo. NFAT elicits this second program of gene expression in large part by binding to a subset of the sites occupied by NFAT during a typical effector response, suggesting that a balance between the two pathways determines the outcome of TCR signaling. Understanding the role of CA-RIT-NFAT1 in T cells

2015-02-13 | E-GEOD-64408 | biostudies-arrayexpress

Direct regulation of T cell exhaustion by NFAT [ChIP-Seq]

2015-02-13 | E-GEOD-64407 | biostudies-arrayexpress

The transcription factor IRF2 drives interferon-mediated CD8+ T cell exhaustion to restrict anti-tumor immunity

Project description:Type I Interferons (IFN-I) stimulate pro-inflammatory programs critical for immune activation, but also induce immune-suppressive feedback circuits that contribute to the failure of cancer control. Yet, how IFN-Is differentially induce these opposing programs remains enigmatic. We establish that the transcription factor Interferon Regulatory Factor 2 (IRF2) is a central feedback molecule attenuating IFN signaling and driving CD8 T cell exhaustion in the tumor microenvironment. IRF2 inhibits CD8 T cell effector function in response to sustained interferon signaling by programming T cell exhaustion. Lineage-specific deletion of IRF2 limits CD8 T cells exhaustion to maintain effector functions, thereby enabling long-term tumor control, and increased responsiveness to immune-checkpoint and adoptive cell therapies. Long-term tumor control by IRF2-deficient CD8 T cells is dependent on continuous integration of both IFN-I and IFN? signals, which in the absence of IRF2, potentiate sustained effector function instead of exhaustion. Thus, IRF2 redirects IFN signalling to drive T cell exhaustion and prevent tumor control.

2022-11-10 | GSE199177 | GEO

Stat5 antagonizes Tox and CD8 T cell exhaustion to foster a durable effector-like state during chronic antigen exposure

Project description:Constitutive Stat5a activity antagonized Tox and rewired CD8 T cells away from exhaustion to acquire a durable effector/NK-like state with superior anti-tumor potential Stat5 fostered TEXint, temporally re-engaging the Stat5 pathway, partially reprogrammed the epigenetic landscape of exhaustion and restored effector-like differentiation and function cell formation and partial re-acquisition of effector-biology during this TEXprog-to-TEXint transition,

2023-08-31 | GSE238239 | GEO

Structure of nucleosome-bound human PBAF complex

Project description:BAF and PBAF are mammalian SWI/SNF family chromatin remodeling complexes that possess multiple histone/DNA-binding subunits and create nucleosome-depleted/free regions for transcription activation. Despite previous structural studies and recent advance of SWI/SNF family complexes, it remains incompletely understood how PBAF-nucleosome complex is organized. Here we determined structure of 13-subunit human PBAF in complex with acetylated nucleosome in ADP-BeF3-bound state. Four PBAF-specific subunits work together with nine BAF/PBAF-shared subunits to generate PBAF-specific modular organization, distinct from that of BAF at various regions. PBAF-nucleosome structure reveals six histone-binding domains and four DNA-binding domains/modules, the majority of which directly bind histone/DNA. This multivalent nucleosome-binding pattern, not observed in previous studies, suggests that PBAF may integrate comprehensive chromatin information to target genomic loci for function. Our study reveals molecular organization of subunits and histone/DNA-binding domains/modules in PBAF-nucleosome complex and provides structural insights into PBAF-mediated nucleosome association complimentary to the recently reported PBAF-nucleosome structure.

2023-03-11 | PXD036708 | Pride

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