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Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [whole blood]

ABSTRACT: Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [whole blood]

PROVIDER: PRJNA894957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22063900.fastq.gz	Fastqsanger.gz
	SRR22064000.fastq.gz	Fastqsanger.gz
	SRR22063901.fastq.gz	Fastqsanger.gz
	SRR22064001.fastq.gz	Fastqsanger.gz
	SRR22063902.fastq.gz	Fastqsanger.gz

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Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy.

Project description:Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy.

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Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [CD8s]

Project description:Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [CD8s]

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Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [CD8s]

Project description:Exhausted CD8 T cells (TEX) are associated with worse outcome in cancer yet better outcome in autoimmunity. However, factors contributing to reduced TEX in autoimmunity are poorly understood. We use two genetically related autoimmune diseases, type 1 diabetes (T1D) and rheumatoid arthritis (RA), to explore these factors. We identify a common human peripheral blood TIGIT+KLRG1+ CD8 TEX population: TIGIT+KLRG1+ CD8 TEX of healthy controls (HC), T1D, and rheumatoid arthritis (RA) subjects share EOMES signature genes, are increased with age and in chronic viral-specific cells and are hyporesponsive in vitro. Consistent with a genetic determinant, TIGIT+KLRG1+ TEX are stable within but vary between individuals. In HC and RA subjects (n>100/cohort), lower levels of EOMES transcriptional modules and TIGIT+KLRG1+ TEX were associated with RA HLA risk alleles (DR0401, 0404, 0405, 0408, 1001) even when considering disease status and CMV seropositivity. TIGIT+KLRG1+ TEX significantly increased in RA HLA risk but not non-risk subjects treated with abatacept (CTLA4Ig); no change in TIGIT+KLRG1+ TEX was observed with adalimumab (anti-TNF) therapy. The DR4 association and selective modulation with abatacept suggests that therapeutic modulation of TEX may be more effective in DR4 subjects and TEX may be indirectly influenced by cellular interactions that are blocked by abatacept.

2023-06-30 | GSE216679 | GEO

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy [whole blood]

2023-06-30 | GSE216678 | GEO

Reduced CD8 T cell exhaustion in DR4 risk subjects is selectively augmented with therapy.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-30 | GSE216680 | GEO

Multiomic profiling of chronically activated CD4+ T cells identifies drivers of exhaustion and metabolic reprogramming

Project description:T-cell exhaustion occurs when T cells are chronically activated, usually in the context of cancer or chronic infection. Exhausted T cells lose effector functions, upregulate inhibitory receptors, and lose proliferation ability. Understanding the mechanisms of T-cell exhaustion is important as it has critical clinical applications, such as checkpoint blockade therapy. CD4+ T cells are understudied in the context of exhaustion, and no large-scale multiomic datasets containing proteomics, phosphoproteomics, or metabolomics exist. We therefor performed a multiomic experiment to profile this cell state using a time course analysis to also capture progression.

2024-11-28 | PXD057703 | Pride

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.

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NFAT5 induction by the tumor microenvironment enforces CD8 T cell exhaustion [ATAC]

Project description:Persistent exposure to antigen during chronic infection or cancer renders T cells dysfunctional. The molecular mechanisms regulating this state of exhaustion are thought to be common in infection and cancer, despite obvious differences in their microenvironments. We discovered that NFAT5, an NFAT family member lacking an AP-1 docking site, is highly expressed in exhausted T cells responding to chronic infection and tumors but is a central player selectively in tumor-induced exhaustion. While NFAT5 overexpression in CD8+ T cells reduced tumor control, NFAT5 deletion improved tumor control by promoting the accumulation of tumor-specific CD8 T cells that expressed less TOX and PD-1 and produced more cytokines specifically among precursor exhausted cells. Conversely, NFAT5 did not promote T cell exhaustion during chronic infection. While NFAT5 expression was induced by TCR triggering, its transcriptional activity was specific to the tumor microenvironment and required hyperosmolarity. NFAT5 thus promotes CD8 T cell exhaustion in a tumor-selective fashion.

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Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [Cut & Run]

Project description:Exhausted CD8 T cells result from chronic antigen stimulation and have reduced ability to clear disease. The epigenetic regulation of the dysfunctional phenotype of exhausted CD8 T cells is a promising avenue for therapies aimed at reversing or preventing CD8 T cell exhaustion. Here, utilizing an in vitro model, we show global increase of the repressive histone modification H3K27me3 in CD8 T cell exhaustion as well as increased gene expression of the subunits of PRC2, the complex responsible for H3K27me3 deposition. H3K27me3 correlated with decreased gene expression and localized to naïve/memory T cell genes in CD8 T cell exhaustion. PRC2 inhibition increased expression of many of these naïve/memory genes while reducing expression of key exhaustion genes. Further, we identified potential enhancers and transcription factors predicted to promote expression of the PRC2 subunits. Our study highlights the importance of the repressive epigenetic landscape of exhausted CD8 T cells as well as a novel role for PRC2 in T cell biology.

2024-10-31 | GSE263937 | GEO

Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion [RNA-seq]

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