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Epigenetic regulation of CD8+ effector T cell differentiation by PDCD5

ABSTRACT: Epigenetic regulation of CD8+ effector T cell differentiation by PDCD5

PROVIDER: PRJNA966175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24403033_1.fastq.gz	Fastqsanger.gz
	SRR24403033_2.fastq.gz	Fastqsanger.gz
	SRR24403034_1.fastq.gz	Fastqsanger.gz
	SRR24403034_2.fastq.gz	Fastqsanger.gz
	SRR24403035_1.fastq.gz	Fastqsanger.gz

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Epigenetic regulation of CD8+ effector T cell differentiation by PDCD5

Project description:Epigenetic modification is critical in the establishment of the transcriptional program for CD8+ effector T cell differentiation. How this is regulated at an early stage before the expression of master transcription factors remains elusive. Here, we identify PDCD5 as an activation-induced molecule that is required for proper differentiation and expansion of antigen-specific CD8+ effector T cells in a chronic viral infection mouse model. Genetic deletion of Pdcd5 diminished effector T cell formation and function, leaving T cell activation, metabolic reprogramming, and memory/exhausted T cell differentiation largely unaffected. At the molecular level, reduced chromatin accessibility and transcription of Tbx21 and its regulated genes were found in Pdcd5-/- CD8+ T cells. We further identify PRDM9 that facilitates the H3K4me3 modification of effector signature genes in CD8+ T cells. The interaction of PDCD5 with PRDM9 promoted the translocation and lysine methyltransferase activity of PRDM9. These data indicate a pivotal role of PDCD5/PRDM9 axis in epigenetic reprogramming at the early stage of effector CD8+ T cell fate determination.

2025-03-25 | GSE231510 | GEO

Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation

Project description:Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation

| PRJNA791324 | ENA

Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (HiChIP)

Project description:Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (HiChIP)

| PRJNA791329 | ENA

Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (RNA-Seq)

Project description:Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (RNA-Seq)

| PRJNA791328 | ENA

Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (ChIP-Seq)

Project description:Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (ChIP-Seq)

| PRJNA791330 | ENA

Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (ATAC-Seq)

Project description:Batf-mediated Epigenetic Control of Effector CD8+ T Cell Differentiation (ATAC-Seq)

| PRJNA791331 | ENA

Global DNA Methylation Remodeling Accompanies CD8 T Cell Effector Function

Project description:In response to acute infection CD8 T cells differentiate into effector cells capable of clearing the antigen. While the transcriptional and functional changes have previously been studied little is known of the epigenetic modifications that accompany this differentiation process. To gain insights into CD8 T cell effector differentiation and the role of epigenetics, we mapped DNA methylation by MeDIP-seq in naive CD8 T cells and day 8 effector CD8 T cells that are induced following an acute infection. We identified hundreds of thousands of differentially methylated regions (DMRs). Promoter DNA methylation inversely correlated with gene expression and DMRs were enriched for functional transcription factor binding sites. These data indicated that DNA methylation is dynamic during CD8 T cell differentiation and provide a map of possible regulatory regions important in this process. Examination of DNA methylation during CD8 T cell differentiation from naïve to day 8 effectors following acute infection

2013-08-18 | E-GEOD-44638 | biostudies-arrayexpress

TLR4 ligands LPS and MPLA differentially regualte effector and memory CD8 T cell differentiation

Project description:Here we implemented a simple dendritic cell (DC)-mediated immunization approach to study the effects of commonly used adjuvants, Toll like receptor (TLR) ligands, on effector CD8 T cell differentiation and memory T cell development. To our surprise, we found that the TLR4 ligand LPS was far more superior to other TLR ligands in generating memory CD8 T cells upon immunization. LPS boosted clonal expansion similar to the other adjuvants, but fewer of the activated CD8 T cells died during contraction, generating a larger pool of memory cells. Intriguingly, monophosphoryl lipid A (MPLA), another TLR4 ligand, enhanced clonal expansion of effector CD8 T cells, but also promoted their terminal differentiation and contraction; thus, fewer memory CD8 T cells formed and MPLA-primed animals were less protected against secondary infection compared to those primed with LPS. Furthermore, gene expression profiling revealed that LPS-primed effector cells displayed a stronger pro-memory gene expression signature, whereas the gene expression profile of MPLA-primed effector cells had aligned closer with terminal effector CD8 T cells. Mice that contain small number of P14 CD8 T cells were immunized with DC-33 either alone or in combination with LPS or MPLA. KLRG1loIL-7Rhi MPECs were purified by FACS sort, and mRNA isolated from MPECs was subjected to whole-genome expression profiling using Illumina MouseWG-6 v2.0 Expression BeadChip.

2014-06-03 | E-GEOD-50764 | biostudies-arrayexpress

Gene expression in LCMV-specific Blimp-1 deficient effector CD8+ T cells compared to wildtype effector CD8+ T cells

Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype. DNA microarray analysis was performed of DbGP33-41 and DbNP396-404 tetramer-positive effector CD8+ T cells FACS-sorted at day 8 post-LCMV infection from four independent samples of either Blimp-1 conditional knockout mice (CKO; Blimp-1flox/flox x GranzymeB-cre+) or wildtype (WT) littermate controls.

2010-08-19 | E-GEOD-17211 | biostudies-arrayexpress

Optimized CD8 effector TL

Project description:Transcriptome analyses of naive, effector and memory CD8 TCRP1A lymphocytes expressing or not an active form of the transcription factor Stat5. TCRP1A CD8 T lymphocytes were activated by their cognate Ag for 72h to induce their differentiation in effector T cells (TCRP1A eTL 72h: 4 replicates S1, S2, S3, S4). In some samples, an active form of Stat5 was introduced (TCRP1A Stat5ca eTL 72h: 2 replicates S9, S10). These 72h activated T cells were either purified and analyzed directly (samples mentioned above) or injected in congeneic hosts and recovered more than 20 days later from the host spleen and lymph nodes: TCRP1A eTL >d20: 2 replicates– S30, S32; TCRP1A Stat5ca eTL >d20: 4 replicates S11, S12, S13, S14). Naive TCRP1A CD8 T lymphocytes (TCRP1A-naive: 4 replicates S33, S34, S35, S36) are included as controls. TCRP1A CD8 T lymphocytes were activated by anti-CD3/CD28. After 24h, an active form of Stat5 was introduced in activated cells. Culture was continued for another 48h to induce their differentiation in effector T cells. These 72h activated T cells were either directly injected in congeneic hosts and recovered more than 14 days later from the host spleen and lymph nodes: T-BetKO Stat5ca >d14: 3 replicates S39, S40, S41.

2013-09-13 | E-GEOD-26945 | biostudies-arrayexpress

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