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WT and Ikaros-deficient follicular B cells stimulated with anti-IgM

ABSTRACT: We have observed that follicular B cells from mice with a hypomorphic mutation (IkL/L) in the Ikzf1 gene (which encodes the Ikaros transcription factor) exhibit an increased proliferative response to anti-IgM stimulation (Kirstetter et al, Eur J Immunol, 32:720-30, 2002). We asked if Ikaros controls the transcriptional response that unfolds after activation, or if differences in the transcriptional landscape of resting B cells could explain the altered response. To this end, we have determined the transcriptome of unstimulated WT and IkL/L follicular B cells, as well as that of cells stimulated for 3h and 12h with anti-IgM. Samples from 2 independent experients were analyzed.

ORGANISM(S): Mus musculus

PROVIDER: GSE75712 | GEO | 2016/01/26

SECONDARY ACCESSION(S): PRJNA305133

REPOSITORIES: GEO

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WT and Ikaros-deficient follicular B cells stimulated with anti-IgM

Project description:We have observed that follicular B cells from mice with a hypomorphic mutation (IkL/L) in the Ikzf1 gene (which encodes the Ikaros transcription factor) exhibit an increased proliferative response to anti-IgM stimulation (Kirstetter et al, Eur J Immunol, 32:720-30, 2002). We asked if Ikaros controls the transcriptional response that unfolds after activation, or if differences in the transcriptional landscape of resting B cells could explain the altered response. To this end, we have determined the transcriptome of unstimulated WT and IkL/L follicular B cells, as well as that of cells stimulated for 3h and 12h with anti-IgM. Samples from 2 independent experients were analyzed. Follicular splenic B cell were sorted from 6-week old WT or IkL/L mice, and stimulated for 3 or 12h with anti IgM, or cultured without anti-IgM for 3h (unstimulated samples) 2 independant experiments were performed

2016-01-26 | E-GEOD-75712 | biostudies-arrayexpress

Ikaros mutant thymic tumors

Project description:The experiment was to compare leukemic T cells from thymic lymphomas from homozygote mice for the IkL/L hypomorphic mutation and non-transformed thymocytes, either of WT or IkL/L genotype. The aim was to identify a gene expression signature specific to the IkL/L tumors. Keywords = thymic lymphoma Ikaros Keywords: other

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Expression data from mouse monocyte- and common- dendritic progenitors (MDP and CDP) from Ikaros mutant in response to gamma-secretase inhibitor (GSI)

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RNAseq of follicular lymphoma patient samples treated with anti-IgM, DC-SIGN or an isotype control

Project description:Here we investigate the relevance of the microenvironment in follicular lymphoma by studying the effect of the lectin DC-SIGN, expressed by macrophages on B-cell receptor activation. We compare the effect of DC-SIGN and anti-IgM stimulation on FL by treating 3 FL samples with 20 μg/ml of goat F(ab’)2 anti-IgM, 20 μg/ml of DC-SIGN-Fc or left untreated for 4 hours at 37°C. Total RNA was extracted using an RNeasy mini kit (Qiagen) and polyA libraries were 75bp PE sequenced on a HiSeq4000 (Ilumina). After gene expression profiling analysis we found that, although DC-SIGN-Fc appears to elicit a weaker transcriptional response than anti-IgM, the responses are closely related and encompass a wide range of canonical BCR response pathways.

2020-01-31 | E-MTAB-8708 | biostudies-arrayexpress

Role of Ikaros in Mature IgM+ B-cells: Studies of IkZnF1-/- and IkZnF4-/- mutant mice [RNA-seq]

Project description:Ikaros is a zinc finger (ZnF) transcription factor critical for B-cell development. The C2H2 zinc finger is the most prevalent DNA-binding motif in the mammalian proteome, with DNA-binding domains usually containing more tandem fingers than are needed for stable sequence-specific DNA recognition. To examine the reason for the frequent presence of multiple zinc fingers, we recently generated mice lacking finger 1 or finger 4 of the 4-finger DNA-binding domain of Ikaros. Each mutant strain exhibited a specific subset of the phenotypes observed with Ikaros null mice, and revealed that different subsets of fingers within multi-finger transcription factors can regulate distinct target genes and biological functions. We here study the effect of these mutants on mature B-cells with transcriptome profiling of sorted IgM+ B-cells from BM of wt and the two ZnF mutants (RNA-Seq).

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Project description:The Autoimmune Regulator (Aire) serves an essential role in T cell tolerance by promoting ‘promiscuous gene expression’ (PGE) in medullary thymic epithelial cells (mTECs). Several disease manifestations associated with Aire-deficiency, some apparently non-autoimmune, along with Aire expression beyond mTECs, suggest that Aire may regulate additional physiological processes. We show that plasmablasts (PBs) and plasma cells (PCs) constitute a principal Aire-expressing population in the spleen, with highest expression in IgM+ cells and lower levels in class-switched PB/PCs. The Aire+IgM+ PB/PC compartment exhibits typical hallmarks of natural IgM secreting cells of extrafollicular origin: it is T cell-independent, exhibits distinct BCR features, and can originate from both peritoneal B1a cells and splenic marginal zone B cells, whereas follicular B cells contribute minimally. While TLR-driven signals initiate PB differentiation as previously described, we find that subsequent stimulation through APRIL or BAFF - but not RANK or CD40 - induces Aire expression, uncovering a novel TNF superfamily axis upstream of Aire induction. Aire does not drive bona fide PGE in these cells, yet cell-intrinsically restrains their numbers, limiting steady-state serum levels of polyreactive IgM. These findings identify Aire as a B lineage-intrinsic regulator of natural IgM, raising the possibility that dysregulation of the IgM+ PB/PC compartment contributes to the pathological consequences of Aire-deficiency.

2026-08-31 | GSE310317 | GEO

B cell response to CD40, Anti-IgM, ELC, IL4, terbutaline and lipopolysaccharide treatment

Project description:Temporal analysis (60, 180, 360 min) of B cells treated with either: CD40 Anti-IgM ELC IL4 Lipopolysaccharide Terbutaline CD40 and IL4 CD40 and Lipopolysaccharide CD40 and Anti-IgM Anti-IgM and ELC Anti-IgM and Terbutaline ELC and Lipopolysaccharide This SuperSeries is composed of the following subset Series: GSE1019: B cell response to Anti-IgM and CD40 treatment GSE1020: B cell response to Anti-IgM and ELC treatment GSE1021: B cell response to Anti-IgM and terbutaline treatment GSE1022: B cell response to CD40 and lipopolysaccharide treatment GSE1023: B cell response to CD40 and IL4 treatment GSE1024: B cell response to ELC and lipopolysaccharide treatment Refer to individual Series

2010-06-09 | E-GEOD-1014 | biostudies-arrayexpress

Mus musculus

Project description:WT and Ikaros-deficient follicular B cells stimulated with anti-IgM

| PRJNA305133 | ENA

TGF-beta1 target genes in human hematopoietic stem/progenitor cells.

Project description:CD34+ hematopoietic stem/progenitor cells were isolated from human cord blood and amplified in vitro for 10-14 days in serum-free medium with specific cytokines (Ju et al., Eur. J. Cell Biol. 82, 75-86, 2003; Hacker et al., Nat. Immunol. 4, 380-386, 2003). Cells were then treated with TGF-beta1 for various periods of time (2, 4, 16 hours) and RNA was prepared and subjected to microarray analysis. Keywords: Response to cytokine treatment for various periods of time.

2006-06-29 | GSE5150 | GEO

Gene expression in WT and Ikaros-deficient LSK cells

Project description:The Ikaros zink finger transcription factor is a critical regulator of the hematopietic system, and plays an important role in the regulation of the development and function of several blood cell lineages. We used microarrays to characterize how Ikaros deficieny affects global transcription in the hematopoietic stem and progenitor cells from wild-type and Ikaros mutant mice. lin- Sca1+ c-Kit+ (LSK) cells, that contains the hematopoietic stem cells and the multipotent progenitor cells, were sorted by FACS from the bone marrow of 6-7 weeks old WT and IkL/L mutant mice. Total RNA extracted from these cells was subjected to transcriptome analysis.

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