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The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells

ABSTRACT: The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells

PROVIDER: PRJNA215367 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12494408_1.fastq.gz	Fastqsanger.gz
	SRR12494408_2.fastq.gz	Fastqsanger.gz
	SRR12494410_1.fastq.gz	Fastqsanger.gz
	SRR12494410_2.fastq.gz	Fastqsanger.gz
	SRR953136_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [ChIP-seq]

Project description:We demonstrate that transcription factor IRF4 is induced in a T cell receptor (TCR) affinity-dependent manner and functions as a dose-dependent regulator of the metabolic function of activated T cells. IRF4 regulates the expression of key molecules required for aerobic glycolysis of effector T cells, and is essential for clonal expansion and maintenance of effector function of antigen-specific CD8+ T cells. Examination of binding sites of transcription factor IRF4 in mouse CD8+ T cells.

2013-08-17 | E-GEOD-49930 | biostudies-arrayexpress

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [RNA-seq]

2013-08-17 | E-GEOD-49929 | biostudies-arrayexpress

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [ChIP-seq]

2013-08-17 | GSE49930 | GEO

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [RNA-seq]

2013-08-17 | GSE49929 | GEO

IRF4 Haploinsufficiency Impairs Affinity Maturation

Project description:IRF4 Haploinsufficiency Impairs Affinity Maturation

| PRJNA767888 | ENA

IRF4 Haploinsufficiency Impairs Affinity Maturation

Project description:Single cell RNA seq (scRNA-seq) has emerged as a powerful tool to determine the composition of heterogeneous cell states in a tissue. We found that Irf4+/- antigen specific B cells were functionally impaired in affinity maturation. The goal of this study was to determine whether Irf4+/- antigen specific B cells exhibited distinct cellular composition compared to wild type cells. Sequence data from 8360 cells revealed a similar distribution and numbers of cell states between cells of Irf4+/- or Irf4+/+ genotypes.

2021-10-04 | GSE185188 | GEO

Dynamic regulation of somatic hypermutation in germinal centers enables rapid B cell clonal expansion without loss of affinity

Project description:In the course of antibody affinity maturation, germinal center (GC) B cells mutate their immunoglobulin (Ig) heavy and light chain genes in a process known as somatic hypermutation (SHM). Panels of mutant B cells with different binding affinities for antigen are then selected in Darwinian fashion, leading to a progressive increase in affinity among the population. As with any Darwinian process, rare gain-of-fitness mutations must be identified while common loss-of-fitness mutations are avoided. Progressive acquisition of mutations therefore poses a risk during large proliferative bursts, when GC B cells go through several cell cycles in the absence of affinity-based selection. Using a combination of in vivo mouse experiments and mathematical modeling, we show that GCs achieve this balance by strongly suppressing SHM during clonal burst-type expansion, so that a large fraction of the progeny generated during such bursts do not deviate from their ancestral genotype. Intravital imaging and image-based cell sorting of a new CyclinE(A)/cyclin-dependent kinase 2 (CDK2) reporter mouse strain showed that B cells actively undergoing proliferative bursts lack the transient CDK2low “G0-like” phase of the cell cycle in which SHM takes place. We propose a model in which inertially cycling B cells largely delay SHM until the G0-like phase that follows their final round of division in the DZ, thus maintaining affinity as they clonally expand in the absence of selection.

2025-03-17 | GSE285185 | GEO

Whole transcriptome analysis for T cell receptor-affinity and IRF4-regulated clonal expansion of T cells.

Project description:Clonal population expansion of T cells during an immune response is dependent on the affinity of the T cell receptor (TCR) for its antigen [1]. However, there is little understanding of how this process is controlled transcriptionally. We found that the transcription factor IRF4 was induced in a manner dependent on TCR-affinity and was critical for the clonal expansion and maintenance of effector function of antigen-specific CD8(+) T cells. We performed a genome-wide expression profiling experiment using RNA sequencing technology (RNA-seq) to interrogate global expression changes when IRF4 was deleted in CD8(+) T cells activated with either a low or high affinity peptide ligand. This allowed us not only to determine IRF4-dependent transcriptional changes but also to identify transcripts dependent on TCR-affinity [2]. Here we describe in detail the analyses of the RNA-seq data, including quality control, read mapping, quantification, normalization and assessment of differential gene expression. The RNA-seq data can be accessed from Gene Expression Omnibus database (accession number GSE49929).

| S-EPMC4536053 | biostudies-literature

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-17 | E-GEOD-49931 | biostudies-arrayexpress

Dynamic regulation of somatic hypermutation in germinal centers enables rapid B cell clonal expansion without loss of affinity

Project description:Dynamic regulation of somatic hypermutation in germinal centers enables rapid B cell clonal expansion without loss of affinity

| PRJNA1201770 | ENA

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