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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: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE49931 | GEO | 2013/08/17

SECONDARY ACCESSION(S): PRJNA215367

REPOSITORIES: GEO

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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

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [RNA-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 gene expression profiles in six types of samples

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 | 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 [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

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

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

| PRJNA215367 | ENA

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

Project description: Not available

| S-EPMC4536053 | biostudies-literature

Metabolic Reprogramming Mediated by the mTORC2-IRF4 Signaling Axis Is Essential for Macrophage Alternative Activation.

Project description: Not available

| S-EPMC5535820 | biostudies-literature

Genomic programming of IRF4-expressing human Langerhans cells.

Project description: Not available

| S-EPMC6965086 | biostudies-literature

Metabolic exhaustion of T cells in chronic infection is mediated by inhibitory receptor PD-1 and T cell receptor dependent transcription factor IRF4

Project description:During chronic stimulation T cells acquire an exhausted phenotype characterized by expression of multiple inhibitory receptors and down-modulation of effector function. While this is required for the protection of the organism from excessive immunopathology, it also prevents successful immunity against persistent viruses or tumor cells. Here we demonstrate that CD8+ T cell exhaustion is characterized by a progressive decline in cellular metabolism. Exhausted T cells exhibit reduced metabolic reserve, impaired fatty acid oxidation and production of mitochondrial reactive oxygen species (ROS). Blockade of inhibitory PD-1/PD-L1 signaling rescued mitochondrial biogenesis, oxidative phosphorylation and ROS production, which was required for efficient restoration of cellular expansion and effector function. Expression of inhibitory receptors and impaired metabolic function was fuled by high amounts of IRF4, BATF and NFAT, which formed a TCR-responsive transcriptional circuit that sustained the transcriptional network responsible for T cell exhaustion.

2018-01-01 | GSE84820 | GEO

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