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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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T-bet regulated genes in KG1 cells

ABSTRACT: T-bet is pivotal for initiation and perpetuation of Th1 immunity. Identification of novel T-bet regulated genes is crucial for further understanding the biology of this transcription factor. By combining siRNA technology with genome-wide mRNA analysis, we sought to identify new T-bet regulated genes in IL-18-activated KG1 cells. KG1 cells were transfected with either control-siRNA (siRNAc) or siRNA targeting T-bet (siRNA-Tbet) and thereafter stimulated with IL-18. Total RNA was evaluated by genome-wide analysis using the Affymetrix GeneChipÂ® Array System.

ORGANISM(S): Homo sapiens

SUBMITTER: Malte Bachmann

PROVIDER: E-GEOD-37595 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

IL-36γ/IL-1F9, an innate T-bet target in myeloid cells.

Bachmann Malte M Scheiermann Patrick P Härdle Lorena L Pfeilschifter Josef J Mühl Heiko H

The Journal of biological chemistry 20121024 50

By concerted action in dendritic (DC) and T cells, T-box expressed in T cells (T-bet, Tbx21) is pivotal for initiation and perpetuation of Th1 immunity. Identification of novel T-bet-regulated genes is crucial for further understanding the biology of this transcription factor. By combining siRNA technology with genome-wide mRNA expression analysis, we sought to identify new T-bet-regulated genes in predendritic KG1 cells activated by IL-18. One gene robustly dependent on T-bet was IL-36γ, a rece ...[more]

PMID: 23095752

Similar Datasets

T-bet regulated genes in KG1 cells

Project description:T-bet is pivotal for initiation and perpetuation of Th1 immunity. Identification of novel T-bet regulated genes is crucial for further understanding the biology of this transcription factor. By combining siRNA technology with genome-wide mRNA analysis, we sought to identify new T-bet regulated genes in IL-18-activated KG1 cells.

2012-10-30 | GSE37595 | GEO

Transcription profiling of human KG1 cells differentiated towards dendritic like cells (DLCs) using PMA and TNF-alpha. Gene expression was compared between undifferentiated KG1 cells and day 4 DLCs

Project description:KG1 cells were differentiated towards dendritic like cells (DLCs) using PMA and TNF-alpha. Gene expression was compared between undifferentiated KG1 cells and day 4 DLCs.

2005-07-20 | E-MEXP-345 | biostudies-arrayexpress

XX-650-23, an inhibitor of CREB-CBP interaction, effect on acute myeloid leukemia cell line

Project description:Analysis of acute myeloid leukemia KG1 cells treated with XX-650-23 (5 mM) for 12hrs. XX-650-23 inhibits proliferation of KG1 cells. Results provides insight into the molecular mechanisms underlying by the inhibitory activity of XX-650-23 on acute leukemia. mRNA profiles of KG1 cells treated with XX-650-23 were generated by deep sequencing. CREB genome binding profiles of KG1 cells treated with XX-650-23 were generated by deep sequencing.

2016-03-26 | E-GEOD-74928 | biostudies-arrayexpress

Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. NaÃ¯ve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection

2016-08-01 | E-GEOD-81189 | biostudies-arrayexpress

The Transcription Factor T-bet Is Induced by Multiple Pathways and Prevents an Endogenous Th2 Cell Program during Th1 Cell Responses

Project description:T-bet is a critical transcription factor for T helper 1 (Th1) cell differentiation. To study the regulation and functions of T-bet, we developed a T-bet-ZsGreen reporter mouse strain, in which GFP faithfully reflects the expression of T-bet. By using this tool, we report that signals elicited by IL-12 and IFNg are redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-bet does not contribute to its own expression when induced by IL-12 and IFNg. While both T-bet and Stat4 are critical for IFNg production, IFNg signaling is dispensable. Strikingly, loss of T-bet results in activation of an endogenous Th2 program in cells expressing T-bet-ZsGreen. Genome-wide analyses suggest T-bet directly induces Th1-related genes but indirectly suppresses Th2-related genes. Our study revealed redundancy and synergy among several Th1-inducing pathways in regulating the expression of T-bet and IFNg, and a critical role of T-bet in suppressing an endogenous Th2 program. RNA-Seq experiments were performed using total RNAs isolated from both wild type and Tbx21-/- Th1 cells in duplicates. Tbet ChIP-seq was performed using wild type Th1 cells. H3K4me1 and H3K27me3 ChIP-seq was performed using both wild type and Tbx21-/- Th1 cells.

2012-10-04 | E-GEOD-38808 | biostudies-arrayexpress

Homo sapiens

Project description:T-bet regulated genes in KG1 cells

| PRJNA161899 | ENA

Genome-wide regulatory analysis reveals T-bet controls Th17 lineage differentiation through direct suppression of IRF4

Project description:The complex relationship between Th1 and Th17 cells is incompletely understood. The transcription factor T-bet is best known as the master regulator of Th1 lineage commitment. However, attention is now focused on the repression of alternate T cell subsets mediated by T-bet, particularly the Th17 lineage. Specifically it has recently been suggested that pathogenic Th17 cells express T-bet and are dependent on IL-23. However, T-bet has previously been shown to be a negative regulator of Th17 cells. We have taken an unbiased approach to determine the functional impact of T-bet on Th17 lineage commitment. Genome-wide analysis of functional T-bet binding sites provides an improved understanding of the transcriptional regulation mediated by T-bet, and suggests novel mechanisms by which T-bet regulates T helper cell differentiation. Specifically, we show that T-bet negatively regulates Th17 lineage commitment via direct repression of the transcription factor interferon regulatory factor-4 (IRF4). An in vivo analysis of the pathogenicity of T-bet deficient T cells demonstrated that Th17 responses were augmented in the absence of T-bet, and we have defined a critical temporal window for T-bet function. The interaction of the two key transcription factors T-bet and IRF4 during the determination of T cell fate choice significantly advances our understanding of the mechanisms underlying the development of pathogenic T cells. ChIP-seq analysis of T-bet in WT and Tbet -/- mice.

2013-12-03 | E-GEOD-40623 | biostudies-arrayexpress

Effect of BAF disruption on T-bet binding in activated CD8+ T cells [ChIP-seq]

Project description:To investigate the role of cBAF in regulation of Tbet binding, polyclonal naive CD8 T cells were stimulated for 48h with anti-CD3, CD28, and hIL-2. Cells were then treated with DMSO, ACBI1, or BRM014 for 6 hours, and treated with recombinant mouse IL-12 for the last two hours of inhibitor treatment. ChIP-seq against T-bet was then performed.

2023-06-13 | GSE228546 | GEO

Tbet vs Eomes [RNA-Seq]

Project description:T-bet and Eomes are related T-box transcription factors that control NK cell development. This study was designed to understand the specific roles of Eomes and T-bet in regulating gene expression. RNAseq data were generated for immature (CD11b- CD27+) and mature (CD11b+ CD27-) NK cells from T-bet KO (Tbet Ho) or control mice (Tbet WT) or from Eomes KO (Eomes Ho) or control mice (NK-Cre). Three samples were generated for each condition (Tri 1, 2, 3).

2021-05-10 | GSE168240 | GEO

Cutting Edge: IL-4, IL-21, and IFN-g Interact to Govern TBET and CD11c Expression in TLR-Activated B Cells

Project description:T-Box Expressed in T cells (TBET) and CD11c expression in B cells is linked with IgG2c isotype switching, virus-specific immune responses, and humoral autoimmunity. However, the activation requisites and regulatory cues governing TBET and CD11c expression remain poorly defined. In this article, we reveal a relationship among TLR engagement, IL-4, IL-21, and IFN-g that regulates TBET expression in B cells. We find that IL-21 or IFN-g directly promote TBET+ expression in the context of TLR engagement. Further, IL-4 antagonizes TBET induction. Finally, IL-21, but not IFN-g, promotes CD11c expression independent of TBET. Using influenza virus and Heligmosomoides polygyrus infections, we show that these interactions function in vivo to determine whether TBET+ and CD11c+ B cells are formed. These findings suggest that TBET+ B cells seen in health and disease share the common initiating features of TLR-driven activation within this circumscribed cytokine milieu.

2016-01-23 | GSE77145 | GEO

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