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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Rachel Rutishauser

PROVIDER: E-GEOD-17211 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional repressor Blimp-1 promotes CD8(+) T cell terminal differentiation and represses the acquisition of central memory T cell properties.

Rutishauser Rachel L RL Martins Gislâine A GA Kalachikov Sergey S Chandele Anmol A Parish Ian A IA Meffre Eric E Jacob Joshy J Calame Kathryn K Kaech Susan M SM

Immunity 20090806 2

During acute infections, a small population of effector CD8(+) T cells evades terminal differentiation and survives as long-lived memory T cells. We demonstrate that the transcriptional repressor Blimp-1 enhanced the formation of terminally differentiated CD8(+) T cells during lymphocytic choriomeningitis virus (LCMV) infection, and Blimp-1 deficiency promoted the acquisition of memory cell properties by effector cells. Blimp-1 expression was preferentially increased in terminally differentiated ...[more]

PMID: 19664941

Similar Datasets

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.

2009-07-22 | GSE17211 | GEO

Transcription profiling of mouse IL-7Rhi/lo effector CD8 T cells on day 6/7 after LCMV armstrong infection

Project description:At the peak of the CD8 T cell response to acture viral and bacterial infections, expression of the Interleukin-7 Receptor (IL-7R) marks Memory Precursor Effector CD8 T Cells (MPECs) from other Short-Lived Effector CD8 T cells (SLECs), which are IL-7Rlo. This study was designed to determine the gene expression differences between these two subsets of effector CD8 T cells. Experiment Overall Design: This study compared IL-7Rhi and IL-7Rlo LCMV-specific P14 Transgenic CD8 T cells, sorted from LCMV armstrong infected recipient mice 6/7 days after infection. Data includes 3 independent replicates for the IL-7Rhi and IL-7Rlo groups.

2008-06-16 | E-GEOD-8678 | biostudies-arrayexpress

Gene expression profile of splenic p14 effector T cells eight days after LCMV infection

Project description:Microarray analyses was employed to determine the gene expression profiles of LCMV-specific p14 CD8+ effector T cells eight days after an acute LCMV Armstrong infection providing a framework to compare and contrast effector function potential of distinct immune cell subsets to CD8+ effector T cells.

2015-06-01 | GSE44410 | GEO

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

Gene expression in WT and Thpok-deficient LCMV-specific effector T cells

Project description:Gene expression of effector CD4+ and CD8+ T cells determined by RNAseq 7 days after LCMV Armstrong infection

2019-08-15 | GSE130474 | GEO

RNAseq analysis of PS+ vs. PS- effector CD8 T cells sorted from spleen of LCMV-Armstrong infected mice

Project description:We report the transcriptional profile of phosphatidylserine (PS) positive and PS negative CD44+CD62L- effector CD8+ T cells from LCMV-Armstrong infected mice sorted from spleens on day5 amd day10 after infection. PS was stained in vivo by injection of MFG-E8-eGFP. PS+ cells acquire PS through binding of extracellular vesicles (EVs). Binding of EVs by effector CD8+ T cells is strongly enhanced during LCMV infection and peaks between day5 and day10 post infection. Effector T cell gene signature is increased in EV+ CD8+ T cells compared to their EV- counterparts.

2023-03-29 | GSE201507 | GEO

Transcriptomic analysis of the early effects of sex steroid ablation on BM LT-HSCs 2 days post surgery.

Project description:Analysis of gene-expression alterations in primitive LT-HSCs as early as 2 days post sex steroid ablation. This study aimed to determine potential intrinsic changes occuring in the LT-HSC population associated with sex steroid ablation (SSA) at a timepoint that preceeded the earliest reported functional hematopoietic enhancements occuring at day 7 post SSA. These results are vital in providing insight into the role of LT-HSCs in initiating SSA-mediated immune regeneration. Total RNA obtained from BM-sorted LT-HSC 2 days after sex steroid ablation compared to sham sex steroid ablation controls.

2015-03-01 | E-GEOD-64841 | biostudies-arrayexpress

Epigenetic modifications induced by Blimp-1 regulate CD8+ T cell memory progression during acute virus infection

Project description:Blimp-1 regulates the overall accumulation of virus-specific CD8+ T cells during acute viral infections. Increased proliferation and survival of Blimp-1-deficient CD8+ T cells is promoted by persistent cytokine responsiveness, resulting from sustained expression of CD25 and CD27. Knockdown of these genes reduced the Blimp-1-deficient CD8+ T cell response. Genome-wide ChIP-sequencing analysis identified CD25 and CD27 genes as direct targets of Blimp-1. At the peak of the anti-viral response, but not earlier, Blimp-1 recruited the histone modifying enzymes G9a and HDAC2 to the Il2ra and Cd27 loci, thereby repressing expression of these genes. In the absence of Blimp-1, the Il2ra and Cd27 genes exhibited enhanced histone H3-acetylation and reduced histone H3K9-trimethylation. These data elucidate a central mechanism by which Blimp-1 acts as an epigenetic regulator, enhancing the numbers of short-lived effector cells while suppressing the development of memory precursor CD8+ T cells. NaM-CM-/ve CD8+ T cells from OT-I TCR transgenic Rag1-/- mice were stimulated with anti-CD3 and anti-CD28 for three days in vitro, in the presence of IL-2 to up-regulate Blimp-1 protein. Genome-wide mapping of Blimp-1 binding in mouse CD8+ T cells was conducted.

2013-10-10 | E-GEOD-48358 | biostudies-arrayexpress

Single-cell gene expression of anti-viral WT and Bcl3-deficient effector T cells

Project description:Single-cell gene expression of effector CD8+ T cells WT or Bcl3-deficient was determined by sRNAseq after LCMV Armstrong infection

2021-01-02 | GSE148660 | GEO

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