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IRF4 Haploinsufficiency Impairs Affinity Maturation

ABSTRACT: IRF4 Haploinsufficiency Impairs Affinity Maturation

PROVIDER: PRJNA767888 | ENA |

REPOSITORIES: ENA

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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.

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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]

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Regulation of bifurcating B cell trajectories by mutual antagonism between IRF4 and IRF8 (RNA-Seq)

Project description:Upon antigen recognition B cells undertake a bifurcated response in which some cells rapidly differentiate into plasmablasts while others undergo affinity maturation in germinal centers (GC). We uncover a double negative feedback loop between interferon regulatory factors IRF4 and IRF8, which regulates the initial bifurcation of activated B cells as well as the GC response. IRF8 dampens BCR signaling, facilitates antigen specific interaction with helper T cells, and promotes selection of high affinity clones while antagonizing IRF4 driven plasmablast differentiation. Genomic analysis reveals concentration dependent action of IRF4 and IRF8 in regulating distinctive gene expression programs. Stochastic modeling suggests that the double negative feedback is sufficient to initiate bifurcating B cell developmental trajectories.

2015-08-25 | GSE70711 | GEO

Regulation of bifurcating B cell trajectories by mutual antagonism between IRF4 and IRF8 (ChIP-Seq)

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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]

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Affinity maturation of antibody against membrane-bound GPCR molecules

Project description:Affinity maturation of antibody against membrane-bound GPCR molecules

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