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TNIK signaling imprints CD8+ T memory formation early after priming

ABSTRACT: TNIK signaling imprints CD8+ T memory formation early after priming

PROVIDER: PRJNA525144 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8655330.fastq.gz	Fastqsanger.gz
	SRR8655331.fastq.gz	Fastqsanger.gz
	SRR8655322.fastq.gz	Fastqsanger.gz
	SRR8655332.fastq.gz	Fastqsanger.gz
	SRR8655323.fastq.gz	Fastqsanger.gz

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TNIK signaling imprints CD8+ T memory formation early after priming

Project description:Purpose: The goal of this study is to compare NGS-derived transcriptome profiling (RNA-seq) of naïve/ effector (D6)/ memory (D80) p14 T cell [wild-type (WT) and Tnik-/- (KO)] isolated form spleen of naïve or adoptively transferred and LCMV-WE immunized mice. Methods: Transcriptomic profiles of splenic naïve wild-type (WT) and Tnik-/- (KO) p14 T cells (8-week-old mice) or splenic effector (D6) and memory (D80) p14 T cells (post adoptive transfer and LCMV-WE immunization) were assessed in duplicates or triplicate by deep sequencing, using Illumina HiSeq 2500. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 30 million sequence reads per sample to the mouse genome (GRCm38 - mm10) and identified expressed transcripts in splenic WT and Tnik−/− p14 T cells. RNA-seq data confirmed stable expression of known housekeeping genes. Differentially expressed genes between the WT and Tnik−/− p14 T cells from naïve, D6 or D80 were identified with a fold change ≥1.5 and p-value <0.05. Hierarchical clustering and gene ontology analysis of differentially expressed genes uncovered genes that may contribute to regulation of stemness, transcriptional regulation, cell cycle regulation, survival and function of T cells. Conclusions: Our study represents the first detailed transcriptome analysis of WT versus Tnik-/- p14 T cells in the context of acute viral infection, with biologic replicates, generated by RNA-seq technology. Our results show that TNIK regulates T cell fate. Evaluation of mRNA content in effector (D6) and memory (D80) p14 T cells revealed that TNIK-deficiency during T cell activation enhances proliferation, terminal differentiation and glycolysis of effector T cells, while compromising steady-state metabolic activity of memory T cells. We conclude that TNIK imprints memory formation early after CD8+ T cell priming.

2020-02-24 | GSE127734 | GEO

TNIK signaling imprints CD8<sup>+</sup> T cell memory formation early after priming.

Project description:Co-stimulatory signals, cytokines and transcription factors regulate the balance between effector and memory cell differentiation during T cell activation. Here, we analyse the role of the TRAF2-/NCK-interacting kinase (TNIK), a signaling molecule downstream of the tumor necrosis factor superfamily receptors such as CD27, in the regulation of CD8+ T cell fate during acute infection with lymphocytic choriomeningitis virus. Priming of CD8+ T cells induces a TNIK-dependent nuclear translocation of β-catenin with consecutive Wnt pathway activation. TNIK-deficiency during T cell activation results in enhanced differentiation towards effector cells, glycolysis and apoptosis. TNIK signaling enriches for memory precursors by favouring symmetric over asymmetric cell division. This enlarges the pool of memory CD8+ T cells and increases their capacity to expand after re-infection in serial re-transplantation experiments. These findings reveal that TNIK is an important regulator of effector and memory T cell differentiation and induces a population of stem cell-like memory T cells.

| S-EPMC7118140 | biostudies-literature

Transcriptional profiling of OT-1 cells during in vitro memory formation after high- or low-affinity priming

Project description:To understand the impact of TCR affinity during priming on memory formation, we performed transcriptional profiling of OT-1 cells at different time points after stimulation with high- or low-affinity ligands. Our findings indicate that low-affinity stimulaation is associated with earlier memory formation.

2020-01-06 | GSE102189 | GEO

Inflammation durably imprints memory CD4+ T cells

Project description:Inflammation durably imprints memory CD4+ T cells

| PRJNA974831 | ENA

Epigenetic basis of CD4 T cel help for memory CD8 T cell formation

Project description:We report here the effects of CD4 T cell help during priming on the acquistion of specific epigenetic program by memory CD8 T cells.

2019-10-23 | GSE118159 | GEO

Transcriptional basis of CD4 T cel help for memory CD8 T cell formation

Project description:CD4+ T-cell help is required for the generation of CD8+ cytotoxic T lymphocyte (CTL) memory. We here reveal how “help” signals delivered during priming impact memory differentiation of CTLs, as informed by genome-wide analyses. “Help” signals promoted the IL-15-dependent maintenance of central memory (TCM) cells. However, they had a much larger impact on the generation of effector memory (TEM) cells and their gene expression program . CD4+ T-cell help created TEM cells that produced Granzyme B and IFNg after antigen-independent recall with IL-12 and IL-18. Furthermore, “helped” memory CTLs expressed the effector program characteristic of “helped” primary CTLs upon recall with MHC class I-restricted antigen only, due to both epigenetic imprinting and sustained mRNA expression of relevant genes . Thus, CD4+ T-cell help delivered during priming creates CD8+ TEM cells with innate and help-independent recall capacities.

2019-10-23 | GSE135141 | GEO

Biotic stress-induced priming and de-priming of transcriptional memory in apple.

Project description:Biotic stress-induced priming and de-priming of transcriptional memory in apple.

| PRJNA507952 | ENA

Biotic stress-induced priming and de-priming of transcriptional memory in Arabidopsis

Project description:Biotic stress-induced priming and de-priming of transcriptional memory in Arabidopsis

| PRJNA507954 | ENA

Kat2a regulates hippocampal memory formation

Project description:Kat2a regulates hippocampal memory formation

| PRJNA231958 | ENA

Rapid proliferation and differentiation impairs the development of memory CD8+ T cells in early life

Project description:Neonates often generate incomplete immunity against intracellular pathogens, although the mechanism of this defect is poorly understood. An important question is whether the impaired development of memory CD8+ T cells in neonates is due to an immature priming environment or lymphocyte-intrinsic defects. Here we show that neonatal and adult CD8+ T cells adopted different fates when responding to equal amounts of stimulation in the same host. While adult CD8+ T cells differentiated into a heterogeneous pool of effector and memory cells, neonatal CD8+ T cells preferentially gave rise to short-lived effector cells and exhibited a distinct gene expression profile. Surprisingly, impaired neonatal memory formation was not due to a lack of responsiveness, but instead because neonatal CD8+ T cells expanded more rapidly than adult cells and quickly became terminally differentiated. Collectively, these findings demonstrate that neonatal CD8+ T cells exhibit an imbalance in effector and memory CD8+ T cell differentiation, which impairs the formation of memory CD8+ T cells in early life mRNA profiles of effector CD8+ T cells from neonatal and adult mice

2014-05-13 | E-GEOD-56575 | biostudies-arrayexpress

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