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ChIP-seq of Mus musculus T helper cell type 2 with retroviral overexpression of Bhlhe40 and Pparg

ABSTRACT: ChIP-seq of Mus musculus T helper cell type 2 with retroviral overexpression of Bhlhe40 and Pparg

PROVIDER: PRJEB28693 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2806272.fastq.gz	Fastqsanger.gz
	ERR2806273.fastq.gz	Fastqsanger.gz
	ERR2806274.fastq.gz	Fastqsanger.gz
	ERR2806275.fastq.gz	Fastqsanger.gz

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Similar Datasets

ChIP-seq of Mus musculus T helper cell type 2 with retroviral overexpression of Bhlhe40 and Pparg

Project description:T cells were extracted from spleens of CBLA mice and activated in vitro with CD3/28 on day 0. They were spinoculated with retroviruses overexpressing a 3xFLAG-gene of interest on day 1. On day 4, BFP-positive (infected) cells were FACS sorted and measured by ChIPmentation. For input ChIP controls, see E-MTAB-6276

2018-11-23 | E-MTAB-7258 | biostudies-arrayexpress

RNA sequencing of Mus musculus T helper cell type 2 with retroviral overexpression of different genes

Project description:RNA sequencing of Mus musculus T helper cell type 2 with retroviral overexpression of different genes

| PRJEB28692 | ENA

Expression data from mouse differentiated Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells

Project description:Microarray data on TH17 cells from Bhlhe40-GFP reporter mice We used microarrays to detail the global programme of gene expression in polarized Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells Purified naÃ¯ve CD4 T cells from spleen were polarized under TH17 condition in vitro. On day 4, cells were stimulated with PMA and ionomycin, and sorted by their Bhlhe40-GFP expression prior to microarray analysis

2016-01-04 | E-GEOD-75407 | biostudies-arrayexpress

Expression data from mouse differentiated Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells

2016-01-04 | GSE75407 | GEO

The transcription factor Bhlhe40 is a switch of inflammatory versus anti-inflammatory Th1 cell fate determination

Project description:Type 1 T helper (Th1) cells play a critical role in host defense against intracellular pathogens and in autoimmune diseases by producing a key inflammatory cytokine interferon (IFN)-γ; some Th1 cells can also be anti-inflammatory through producing IL-10. However, the molecular switch for regulating the differentiation of inflammatory and anti-inflammatory Th1 cells is still elusive. Here we show that Bhlhe40-deficient CD4 Th1 cells produced less IFN-γ but substantially more IL-10 than wild type Th1 cells. Bhlhe40-mediated IFN-γ production was independent of transcription factor T-bet regulation. Mice with conditional deletion of Bhlhe40 in T cells succumbed to Toxoplasma gondii infection and blockage of IL-10 signaling during infection rescued these mice from death. Thus, our results demonstrate that transcription factor Bhlhe40 is a molecular switch for determining the fate of inflammatory and anti-inflammatory Th1 cells.

2018-05-10 | GSE103173 | GEO

Cell‐intrinsic functions of Bhlhe40 in activated B cells and TFH cells restrain the GC reaction and prevent lymphomagenesis

Project description:The generation of high-affinity antibodies against pathogens and vaccines requires the germinal center (GC) reaction – a process that relies on a complex interplay between specialized effector subsets of B and CD4 T lymphocytes – GC B cells and T follicular helper (TFH) cells. Intriguingly, several key positive regulators of the GC reaction are common for both cell types. Here, we report that the transcription factor Bhlhe40 is a crucial cell-intrinsic negative regulator affecting both the B and T cell sides of the GC reaction. In activated CD4 T cells, Bhlhe40 was required to restrain proliferation thus limiting the number of TFH cells. In B cells, Bhlhe40 executed its function in the first days after immunization by selectively restricting the generation of the earliest GC B cells but not of early memory B cells or plasmablasts. Conditional Bhlhe40 inactivation confirmed cell-autonomous functions of Bhlhe40 in both GC B and TFH cells, while the GC phenotype was further enhanced upon loss of Bhlhe40 in both cell types. This negative regulation of the GC reaction by Bhlhe40 was of crucial importance, as Bhlhe40-deficient mice with progressing age succumbed to a B cell lymphoma characterized by the accumulation of monoclonal GC B-like cells and polyclonal TFH cells in various tissues.

2021-10-25 | GSE186457 | GEO

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [BHLHE40 CUT&RUN]

Project description:NK cells represent a cellular component of the mammalian innate immune system, and mount rapid responses against viral infection, including the secretion of the potent anti-viral effector cytokine IFN-g. Following mouse cytomegalovirus (MCMV) infection, Bhlhe40 was the most highly induced transcription factor in NK cells among the basic helix-loop-helix family. Bhlhe40 upregulation in NK cells depended upon IL-12 and IL-18 signals, with the promoter of Bhlhe40 enriched for STAT4 and the permissive histone H3K4me3, and STAT4-deficient NK cells showing an impairment of Bhlhe40 induction and diminished H3K4me3. Transcriptomic and protein analysis of Bhlhe40-deficient NK cells revealed a defect in IFN-g production during MCMV infection, resulting in diminished protective immunity following viral challenge. Finally, we provide evidence that Bhlhe40 directly promotes IFN-g by binding throughout the Ifng loci in activated NK cells. Thus, our study reveals how STAT4-mediated control of Bhlhe40 drives protective IFN-g secretion by NK cells during viral infection.

2023-09-13 | GSE242900 | GEO

Placental PPARg-Regulated Genes

Project description:Robust identification of placental PPARg target genes via mutliple PPARg-dependence criteria. Integration of differential expression data from Pparg-null, Rxra-null, Med1-nul and Ncoa6-null placentas and from WT and Pparg-null Trophoblast stem cells (TSC) differentiated for 2 or 4 days in the presence or absence of the PPARg agonist Rosiglitazone (Rosi).

2012-07-10 | GSE39233 | GEO

Microarray data for Bhlhe40-sufficient and -deficient resident macrophages

Project description:Most tissue-resident macrophage populations develop during embryogenesis, self-renew in the steady state, and can expand during type 2 immunity. Whether shared mechanisms regulate macrophage proliferation in homeostasis and disease is unclear. We found that the transcription factor Bhlhe40 was cell-intrinsically required in large peritoneal macrophages (LPMs) for self-renewal and maintenance, but was not required in other resident macrophages. Bhlhe40 was selectively necessary in LPMs for proliferation, but not polarization, in response to IL-4. During a helminth infection, Bhlhe40 was required for normal LPM cell cycling. Bhlhe40 repressed the expression of Maf and Mafb and directly promoted expression of cell cycle-related transcripts to enable proliferation of LPMs. Genomic sites bound by Bhlhe40 in LPMs included some co-bound by the macrophage lineage-determining factor PU.1 and others uniquely bound by Bhlhe40, including Maf and cell cycle-related loci. Our findings demonstrate a tissue-specific control mechanism regulating resident macrophage proliferation in homeostasis and type 2 immunity.

2019-04-30 | GSE125727 | GEO

BHLHE40 Orchestrates TL1A-Driven ILC3 Effector Programs and RORγt⁺ APC-Mediated Tolerance

Project description:A central feature of the intestinal immune system is the ability to protect against pathogens while maintaining antigen-specific tolerance to the gut bacteria that coat its surface. Here, we identified Bhlhe40 as a central regulator of both ILC3- and ROR t⁺ APC-dependent mucosal immunity. TL1A stimulation and inflammatory bowel disease both enhance Bhlhe40 expression in intestinal ILC3s. Basal Bhlhe40 expression in ILC3s is essential for efficient transcription of cytokine effectors and maintenance of mucosal immunity, whereas TL1A-induced upregulation of Bhlhe40 further amplifies these effects. Bhlhe40 is also highly expressed in ROR t⁺ APCs, where it is required for optimal generation of antigen-specific Tregs. Together with the colonic microbiota, Bhlhe40 regulates expression of the co-stimulatory molecule Tnfsf4 (OX40L), which is necessary for the induction of Helicobacter hepaticus-specific Tregs. These findings reveal a previously unrecognized role for Bhlhe40 in orchestrating intestinal ILC3 responses and promoting Bhlhe40-dependent co-stimulatory signals in ROR t⁺ APCs that coordinate antigen-specific tolerance.

2026-07-06 | GSE279193 | GEO

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