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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.

2021-10-04 | GSE185188 | GEO

B Cell-Intrinsic IRF4 Haploinsufficiency Impairs Affinity Maturation.

Project description: Not available

| S-EPMC9085970 | biostudies-literature

CFP1 promotes germinal center affinity maturation and restrains and memory B cell differentiation through H3K4me3 modulation

Project description:Affinity maturation and differentiation of B cells in the germinal center (GC) are tightly controlled by epigenetically regulated transcription programs but the underlying mechanisms are only partially understood. Here we show that CFP1, an integral component of the histone methyltransferase complex Set1A/B, is critically required for GC responses. CFP1 deficiency in activated B cells greatly impairs GC formation with diminished proliferation, somatic hypermutation and affinity maturation. Mechanistically, CFP1 deletion reduces H3K4me3 marks at a subset of cell cycle and GC-related genes and impairs their transcription. Importantly, CFP1 promotes the expression of transcription factors MEF2B and OCA-B and the Bcl6 enhancer-promoter looping for its efficient induction. Accordingly, CFP1-deficient GCB cells upregulate IRF4 and preferentially differentiate into plasmablasts. Furthermore, CFP1 ablation upregulates a panel of pre-memory genes with elevated H3K4me3 and leads to markedly expanded memory B populations. In summary, our study reveals that CFP1-safeguarded epigenetic regulation ensures proper dynamics of GCB cells for affinity maturation and prevents the pre-mature exit from GC as memory cells.

2025-08-02 | GSE288059 | GEO

IRF4 haploinsufficiency in a family with Whipple’s disease

Project description:IRF4 haploinsufficiency in a family with Whipple’s disease

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Haploinsufficiency of BCL6 impairs follicular T-B interactions

Project description:Haploinsufficiency of BCL6 impairs follicular T-B interactions

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Regulated somatic hypermutation enhances antibody affinity maturation

Project description:Germinal centers (GCs) are microenvironments where B cells undergo affinity maturation through somatic hypermutation (SHM) and selection by T follicular helper (TFH) cells. While SHM introduces mutations at a fixed rate (~1x10⁻³ per base pair per division), most mutations are deleterious, particularly in high-affinity B cells undergoing many divisions. This study tests a theoretical model suggesting that high-affinity B cells optimize maturation by dividing more but mutating less per division. Data from mice immunized with SARS-CoV-2 or a model antigen support the model, showing that high-affinity B cells shorten their G0/G1 phases and reduce mutation rates, safeguarding their lineages and improving affinity maturation outcomes.

2025-01-27 | GSE287123 | GEO

Regulated somatic hypermutation enhances antibody affinity maturation

Project description:Regulated somatic hypermutation enhances antibody affinity maturation

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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]

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

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

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