RNA-SEQ analysis of CD4+ T cells in presence or absence of Ikaros.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE157810 | GEO | 2021/04/26
REPOSITORIES: GEO
Similar Datasets
Project description:We found that Ikaros is critical to limit the expression of pro-inflammatory cytokines in TCR/CD28-activated CD4+ T cells. To understand if Ikaros could modify the chromatin accessibility in regions controling the expression of these pro-inflammatory genes, we examined the chromatin state in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies for 1 and 2 days, from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+), using the ATAC-seq approach.
2021-04-26 | GSE157812 | GEO
Project description:The aim of the project is to determine the binding sites of Ikaros in CD4+ T cells. To perform this, CD4 naive T cells (CD4 TN; d0) either rested or activated with anti-CD3+anti-CD28 Abs for 1 day (Th0 d1) were subjected to a ChIP using anti-Ikaros Ab followed by high throughput sequencing.
2021-04-26 | GSE157811 | GEO
Project description:We found that CD4+ T cells require Ikaros to promote IL-17 production when cultured in Th17 conditions. To understand why Ikaros null T cells do not produce IL-17, we analyzed the transcriptome of WT vs. Ikaros null naive CD4+ T cells both resting (day 0) or activated with anti-CD3 plus anti-CD28 antibodies, IL-6, TGFb1 and neutralizing anti-IFNg and anti-IL-4 antibodies (Th17 condition) for 1 or 2 days. Samples from 3 independent experiments were analyzed.
2021-04-26 | GSE133878 | GEO
Project description:Sanchez2017 - Inflammatory responses during acute hyperinsulinemia
This model is described in the article:
The CD4+ T cell regulatory
network mediates inflammatory responses during acute
hyperinsulinemia: a simulation study
Mariana E. Martinez-Sanchez, Marcia
Hiriart, Elena R. Alvarez-Buylla
BMC Systems Biology
Abstract:
Obesity is frequently linked to insulin resistance, high
insulin levels, chronic inflammation, and alterations in the
behaviour of CD4+ T cells. Despite the biomedical importance of
this condition, the system-level mechanisms that alter CD4+ T
cell differentiation and plasticity are not well understood. We
model how hyperinsulinemia alters the dynamics of the CD4+ T
regulatory network, and this, in turn, modulates cell
differentiation and plasticity. Different polarizing
microenvironments are simulated under basal and high levels of
insulin to assess impacts on cell-fate attainment and
robustness in response to transient perturbations. In the
presence of high levels of insulin Th1 and Th17 become more
stable to transient perturbations, and their basin sizes are
augmented, Tr1 cells become less stable or disappear, while
TGF? producing cells remain unaltered. Hence, the model
provides a dynamic system-level framework and explanation to
further understand the documented and apparently paradoxical
role of TGF? in both inflammation and regulation of immune
responses, as well as the emergence of the adipose Treg
phenotype. Furthermore, our simulations provide new predictions
on the impact of the microenvironment in the coexistence of the
different cell types, suggesting that in pro-Th1, pro-Th2 and
pro-Th17 environments effector and regulatory cells can
coexist, but that high levels of insulin severely diminish
regulatory cells, especially in a pro-Th17 environment. This
work provides a first step towards a system-level formal and
dynamic framework to integrate further experimental data in the
study of complex inflammatory diseases.
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2017-06-27 | MODEL1606020000 | BioModels
Project description:The goal of this experiment is to define how lack of Ikaros impacts gene expression in mature CD4 T cells, both in the resting and activated state. To do this, a conditional knockout mouse model was generated using Cre/lox technology. The floxed allele was designed such that the last translated exon and 3' UTR of the Ikaros gene (Ikzf1) are deleted in mature T cells (mediated by distal Lck-driven Cre). CD4 T cells from mice with floxed alleles that did not express Cre (Cre-) and those that did express Cre (Cre+) were analyzed.
2018-12-12 | GSE119067 | GEO
Project description:To investigate the transcriptomic changes of Th0 or Th17 cells by IPMK, naïve CD4 T cells of Ctrl and IPMK-KO mice were sorted by FACS and differentiated into Th0 or Th17 cells and RNA seq was performed.
2023-05-17 | GSE203137 | GEO
Project description:This dataset comprises expression profiles from 3 thymic lymphomas from Ikaros deficient mice (IkL/L model, see Dumortier et al, Mol. Cell. Biol. 26, 209-220, 2006 for a description of the tumor model) and 3 thymic lymphomas from IkL/L mice that harbor a mutation of the Notch1 gene (deletion of floxed sequences comprising the promoter and exon 1 with the CD4-Cre transgene). The results from this experimpent is that the expression of Notch target genes was unexpectedly not altered in the tumors with the Notch1 deletion. This result is explained by the activation of a cryptic 3' Notch1 promoter in the deleted tumors, which leads to constitutive Notch1 activation. These results are described in the following publication: R Jeannet, J Mastio, B Macias-Garcia, A Oravecz, T Ashworth, AS Geimer-Lelay, B Jost, S Le Gras, J Ghysdael, T Gridley, T Honjo, F Radtke, J Aster, S Chan and P Kastner. Oncogenic activation of the Notch1 gene in mouse T-cell leukemia by deletion of its promoter. Blood, in press (2010) Primary thymic tumors from 3 IkL/L Notch1+/+ CD4-Cre+ mice (aged 18-20 weeks) were compared to similar tumors from 3 IkL/L Notch1f/f CD4-Cre+ mice (aged 8-10 weeks).
2010-09-03 | E-GEOD-23972 | biostudies-arrayexpress
Project description:Genome-wide binding of Ikaros in naive CD4+ T cells and Th0 at day1
| PRJNA662892 | ENA
Project description:Mouse spleen CD4+CD44LowCD62LHigh cells were stimulated with 2ug/ml anti-CD3(eBioscience), 2ug/ml anti-CD28 (eBioscience) in the presence (Th17 condition) or absence (Th0 condition) of hTGFb-1 (1ng/ml eBioscience), mouse IL-6(10ng/ml eBioscience). Cells were collected after 24 hourÕs culture using RNAeasy columns (Qiagen) for total RNA isolation. Isolated total RNA from Th0 and Th17 conditioned cells were submitted for the microarray gene transcription comparison analysis using Affymetrix Mouse 430A 2.0 array chips.
2008-12-21 | E-TABM-583 | biostudies-arrayexpress
Project description:Ikaros is an essential regulator of lymphopoiesis. Here, we studied the B-cell-specific function of Ikaros by conditional Ikzf1 inactivation in pro-B cells. B-cell development was arrested at an aberrant ‘pro-B’ cell stage characterized by increased cell adhesion and loss of pre-B cell receptor signaling. Ikaros was found to activate genes coding for pre-BCR signal transducers and to repress genes involved in the downregulation of pre-BCR signaling and upregulation of the integrin signaling pathway. Unexpectedly, derepression of Aiolos expression could not compensate for the loss of Ikaros in pro-B cells. Ikaros differentially controlled active chromatin at promoters and enhancers of repressed and activated target genes. Notably, Ikaros binding and target gene expression was dynamically regulated at distinct stages of early B-lymphopoiesis. 16 RNA-Seq samples in pre-proB cells (4 replicates, for each 2 controls and 2 experimental samples); 4 RNA-Seq samples in pro-B cells in Rag2-/- backgrounds (Ikzf1 deleted versus non deleted, 2 replicates each); 4 RNA-Seq samples in c-Kit high pro-B cells (Ikzf1 deleted versus non deleted, 2 replicates each); 4 RNA-Seq samples in pro-B cells (Ikzf1 deleted versus non deleted, 2 replicates each); 2 RNA-Seq samples pre-B cells wild type; 8 chromatin ChIP-Seq samples (4x H3K9ac, 4x H3K4me3, Ikzf1 deleted/non deleted, two replicates each).; 4 Transcription factor ChIP-Seq samples in pro-B cells; 1 Transcription factor ChIP-Seq samples in DP-T cells; 1 Transcription factor ChIP-Seq samples in pre-pro-B cells; 2 Mi-2b Chip-Seq samples (Ikzf1 deleted versus non deleted); 1 ChIP-Seq input track for pro-B cells; 1 ChIP-Seq input track for DP-T cells
2014-02-09 | E-GEOD-53595 | biostudies-arrayexpress