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Transcription profiling by array of mouse irf4 knockout mature splenic B cells against wild type controls from littermates

ABSTRACT: Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

ORGANISM(S): Mus musculus

SUBMITTER: Ulf Klein

PROVIDER: E-GEOD-51932 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells and cultures with mitogens in vitro. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

2015-11-01 | E-GEOD-74287 | biostudies-arrayexpress

Bulk RNAseq for B1a B cells of WT and IRF4 T95R mutant mice

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RNA-sequencing of wild-type and IRF4-deficient splenic cDC2s

Project description:We analyzed the transcriptome differences of wild-type and IRF4-deficient (CD11c-cre x Irf4fl/fl) type-2 conventional dendritic cells (cDC2s) in spleen. Wild-type or IRF4-deficient (CD11c-cre x Irf4fl/fl) bone marrow cells were transferred into lethal irradiated CD45.1 mice. 8 weeks later, splenic cDC2s were purified and prepared for RNA-seq analysis. Three technical repeats of ~10^5 cells per sample from each of one mouse were included. CD97 was downregulated in IRF4-deficient cDC2s. GSEA showed that upregulated and downregulated genes in CD97-deficient cells were strongly enriched in IRF4-regulated genes. These data are in accord with CD97 acting within the IRF4 gene-expression network.

2022-03-23 | GSE188832 | GEO

A new type of pathogenic transcription factor mutation targeting interferon regulatory factor 4 (IRF4) in human lymphoma

Project description:We report the characterization of a recurrent somatic mutation c.295T>C (p.C99R) in the Interferon Regulatory Factor 4 (IRF4) gene in human lymphoma in the α3-recognition helix of the IRF4 DNA-binding domain. IRF4-C99R fundamentally alters IRF4 DNA-binding, combining loss-of-binding at canonical IRF motifs and neomorph gain-of-binding at canonical and non-canonical IRF composite elements (CEs). IRF4-C99R thoroughly modifies IRF4 function, blocking IRF4-dependent plasma cell induction, and specifically up-regulating lymphoma-specific genes in a degenerate Activator Protein-1 (AP-1)-IRF-CE (AICE)-dependent manner.

2023-07-21 | E-MTAB-12522 | biostudies-arrayexpress

IRF4, a master transcription factor, regulates genes involved in BCR signaling, antigen processing and presentation, and GC development [expression array]

Project description:Interferon regulatory factor 4 (IRF4) is a master transcription factor required for the maturation of germinal center B cells that eventually develop into antibody secreting plasma cells and memory B cells. IRF4-deficient mice exhibit a profound reduction in serum immunoglobulin levels. In spite of wealth of the information relating to IRF4 and B cell biology, little is known about the intricate molecular details of the role of this transcription factor during B cell development. We therefore examined the genome-wide targets of IRF4 by ChIP-chip analysis in GC derived BL2 Burkittâs lymphoma cells. ChIP studies were further supplemented by whole genome expression analysis after shRNA-mediated knockdown of IRF4. Our study revealed that IRF4 regulates expression of genes important for a) BCR signaling b) antigen processing and presentation by MHC. In addition we found that IRF4 possibly in some way involved to regulate LTA, LTB and CXCR5 those involved in immune system development, particularly light zone development related genes such as FDC clustering regulating and IL21R and IL10 who are involved in B cell development.. On the other hand, IRF4 suppressesd genes in the oxidative phosphorylation pathway. Our findings illuminate hitherto unexplored roles of IRF4 in GC B cell development. BL2 Burkitt's lymphoma-derived B cells were infected with lentivirus expressing shRNA for IRF4 or control, and total RNA was subjected to Illumina BeadsExpression Arrays analysis.

2015-12-15 | E-GEOD-64269 | biostudies-arrayexpress

Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells.

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Essential role of IRF4 and MYC signaling for survival of anaplastic large cell lymphoma survival

Project description:Three ALCL cell lines DEL, FEPD and K299 were induced with an IRF4-specific shRNA for up to 96 hours. The three ALCL cell lines DEL, FEPD and K299 were induced with an IRF4-specific shRNA for four durations and compared with the corresponding not-induced control.

2015-01-03 | E-GEOD-59747 | biostudies-arrayexpress

Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells.

2015-11-01 | GSE74287 | GEO

Transcriptional regulation of germinal center B and plasma cell fates by dynamical control of IRF4 (expression)

Project description:Temporal analysis of B cell activation in vitro using CD40L and IL-2/4/5 cytokines in wild type Irf4+/+ B cells or in mutant Irf4-/- B cells harboring a tet-inducible allele of Irf4. IRF4 expression was restored, or not, in the Irf4-/- background by culturing in the presence of low or high concentrations of doxycycline. The results provide insight in the role of IRF4 expression levels in coordinating different programs of B cell differentiation. Resting mature peripheral primary B cells were enriched from the spleens of Irf4+/+ or Irf4-inducible mice on the Irf4-/- background. We sought to compare gene expression profiles of wild type and Irf4 mutant B cells in response to mitogens that promote the differentiation of the B cells into plasma cells and cells that have undergone class switch recombination. Day 0 samples represent RNA analysis of unstimulated cells, whereas Day 1 and Day 3 samples represent analysis of stimulated cells in culture. For stimulation, cells were cultured with insect cell purified CD40L and IL-2/4/5 cytokines for the indicated days. In the case of doxycycline-mediated rescue of IRF4 expression, doxycycline was added at predefined low and high concentrations that yield low or high numbers of plasma cells, respectively (see Molecular Systems Biology 7:495). Each replicate represents analysis of B cells from an individual mouse. Of the three replicates in each group, two were performed in parallel and one was performed at a different time. All cells were lysed using Trizol and total RNA was purified according to manufacturer's suggestions. The high quality of the RNA was confirmed using Agilent Bioanalyzer 2100 system. 250ng of RNA was then processed into biotinylated cRNA according to standard procedures and used to hybridize to Affymetrix 430 2.0 arrays. Signal intensities were normalized using the D-Chip algorithm (PM-only model) and the output was used to quantify differential gene expression between groups.

2013-05-04 | E-GEOD-46606 | biostudies-arrayexpress

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