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CUT&Tag ChIP-seq analysis of BATF in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

ABSTRACT: CUT&Tag ChIP-seq analysis of BATF in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

PROVIDER: PRJNA630193 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14713285_1.fastq.gz	Fastqsanger.gz
	SRR14713285_2.fastq.gz	Fastqsanger.gz
	SRR14713286_1.fastq.gz	Fastqsanger.gz
	SRR14713286_2.fastq.gz	Fastqsanger.gz
	SRR14713287_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

CUT&Tag ChIP-seq analysis of BATF in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

Project description:During chronic viral infection, pathogen-specifc CD8+ T cells develop into three main phenotypically and functionally distinct subsets: TCF1hi progenitor, PD-1hi exhausted, and recently identied CX3CR1+ cytotoxic effector cells. Although genetic programs governing progenitor and exhausted subset formation have been well-studied, how CX3CR1+ effector CD8+ T cell differentiation is transcriptionally and epigentically regulated remains elusive. In this study, our single cell transcriptomics and epigenetic assays revealed that three subsets of virus-specific cells were governed by distinct gene regulatory networks (GRNs) and epigenetic landscapes. Computational analyses demonstrated a striking similarity between the CX3CR1+ subset and short-live effector cells (SLECs) from acute LCMV infection. Consistently, genetic deletion of T-bet (Tbx21) significantly diminished the formation and function of the CX3CR1+ subset. Importantly, we identify that the transcription factor (TF) BATF is required to maintain a permissive chromatin structure that allows differentiation transition from TCF1+ progenitor to CX3CR1+ effector cells. Intriguingly, haplodificiency of BATF in CD8+ T cells abolished CX3CR1+ effector subset formation. Lastly, we found that BATF directly bound to key genetic regions such as Tbx21 and modulated their enhancer accessibility to facilitate progenitor to CX3CR1+ effector cell transition. These mechanistic insights can be harnessed to overcome T cell exhaustion in treating chronic infections and cancer.

2021-06-02 | GSE149796 | GEO

Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

2021-05-22 | GSE149752 | GEO

Genome-wide maps of histone modifications in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

2021-05-22 | GSE149810 | GEO

Identification of a T-bet hi Quiescent Exhausted CD8 T Cell Subpopulation That Can Differentiate into TIM3 + CX3CR1 + Effectors and Memory-like Cells

Project description:Persistent Ag induces a dysfunctional CD8 T cell state known as "exhaustion" characterized by PD-1 expression. Nevertheless, exhausted CD8 T cells retain functionality through continued differentiation of progenitor into effector cells. However, it remains ill-defined how CD8 T cell effector responses are sustained in situ. In this study, we show using the mouse chronic lymphocytic choriomeningitis virus infection model that CX3CR1+ CD8 T cells contain a T-bet-dependent TIM3-PD-1lo subpopulation that is distinct from the TIM3+CX3CR1+PD-1+ proliferative effector subset. The TIM3-CX3CR1+ cells are quiescent and express a low but significant level of the transcription factor TCF-1, demonstrating similarity to TCF-1hi progenitor CD8 T cells. Furthermore, following the resolution of lymphocytic choriomeningitis virus viremia, a substantial proportion of TCF-1+ memory-like CD8 T cells show evidence of CX3CR1 expression during the chronic phase of the infection. Our results suggest a subset of the CX3CR1+ exhausted population demonstrates progenitor-like features that support the generation of the CX3CR1+ effector pool from the TCF-1hi progenitors and contribute to the memory-like pool following the resolution of viremia.

2021-04-13 | GSE148497 | GEO

Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

Project description:Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

| PRJNA630086 | ENA

ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.

2014-03-02 | E-GEOD-54191 | biostudies-arrayexpress

Comparison of gene expression profiles of naÃ¯ve and in vitro effector CD8+ T cells from wild-type and BATF-/- mice

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. P14 TCR transgenic CD8+ T cells from wild-type or BATF-/- mice were examined either as naÃ¯ve cells or after 3 days of in vitro stimulation with antibodies to CD3 and CD28 in the presence of IL-2

2014-03-02 | E-GEOD-54215 | biostudies-arrayexpress

Transcription profiling of mouse naive, effector, memory and exhausted virus-specific CD8 T cells after chronic viral infection

Project description:CD8 T cells normally differentiate from resting naÃ¯ve T cells into function effector and then memory CD8 T cells following acute infections. During chronic viral infections, however, virus-specific CD8 T cells often become exhausted. We used microarrays to examine the gene expression differences between naive, effector, memory and exhausted virus-specific CD8 T cells following lymphocytic choriomeningitis virus infection. Experiment Overall Design: Three or four independent samples were sorted by flow cytometry for each cell type (naive, effector, memory and exhausted) virus-specific CD8 T cells. RNA was extracted and hybridized to Affymetrix microarrays.

2008-06-16 | E-GEOD-9650 | biostudies-arrayexpress

Genome-wide maps of histone modifications in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

Project description:Genome-wide maps of histone modifications in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

| PRJNA630212 | ENA

Tumor-infiltrating, adoptively transferred BATF-overexpressing CD8 T cells analyzed via bulk RNA-seq

Project description:In cancer, tumor infiltrating lymphocytes (TILs) often differentiate into dysfunctional states, re-sembling exhausted T cells that arise in chronic viral infections. The dysfunctional state of exhaustion in CD8 T cells is characterized by diminished effector function, namely decreased cytotoxic activity and reduced expression of effector molecules, such as granzyme B. BATF is a transcription factor (TF) known to promote the differentiation of effector CD8 T cells in the chronic viral infection model; however, its role in cancer is not well studied. Using bulk RNA-sequencing (bulk RNA-seq), we identified that BATF-overexpression in tumor-specific CD8 T cells exhibited enrichment for a gene set upregulated in early effector CD8 T cells compared to late exhausted CD8 T cells. Notably, BATF overexpression enhanced the gene expression of various activation markers, costimulatory molecules, effector molecules, chemokine receptors, and other transcription factors, including Hif1a. Additionally, GSEA analysis revealed that BATF-overexpressing CD8 T cells were negatively enriched for Reactome pathways of cellular responses to stress as well as stress-induced senescence. Collectively, our findings support BATF as a key regulator of effector CD8 T cell activity and function within the tumor and shed light on potential pathways BATF may upregulate to facilitate effective tumor control.

2021-10-26 | GSE165420 | GEO

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