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Transcriptome analysis of CD4+ T cells differentiated from wild-type and CD4cre IRF8flox mice

ABSTRACT: We report that the Th9 differenciation program is alterated in absence of IRF8 protein

ORGANISM(S): Mus musculus

PROVIDER: GSE99166 | GEO | 2017/10/02

SECONDARY ACCESSION(S): PRJNA387455

REPOSITORIES: GEO

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Chromatin interaction analysis of transcription factors and IRF8 in CD4+ T cells differentiated from wild-type mice

Project description:We report that the IRF8 protein is able to interact with chromatin during Th9 differenciation

2017-10-02 | GSE99165 | GEO

Transcriptome analysis of Th9 CD4+ T cells differentiated with or without Il-1beta

Project description:We report that the Th9 differenciation program is boosted in presence of Il-1beta

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Transcriptome analysis of Th9 CD4+ T cells differentiated with or without Il-1beta

Project description:We report that the Th9 differenciation program is boosted in presence of Il-1beta Examination of the expression profile of Th9 CD4+ T cells after 1 hour and 3 days of differentiation and after in vivo injection

2014-05-23 | E-GEOD-54697 | biostudies-arrayexpress

Transcriptome analysis of Th2 CD4+ T cells differentiated from wild-type and NLRP3KO mice

Project description:We report that the Th2 differentiation program is altered in absence of NRLP3 protein

2015-05-12 | GSE54561 | GEO

Transcriptome analysis of Th2 CD4+ T cells differentiated from wild-type and NLRP3KO mice

Project description:We report that the Th2 differentiation program is altered in absence of NRLP3 protein Examination of the expression profile of Th2 CD4+ T cells after 3 and 6 days of differentiation

2015-05-12 | E-GEOD-54561 | biostudies-arrayexpress

Effect of IL-7 on CD4+ T cell and Th9 cells

Project description:We found that IL-7 pretreatment enhanced Th9 differentiation. To clarify the underlying mechanisms, we examine the gene expression profiles of CD4+ T cell and Th9 cells with or without IL-7 pretreatment. In Th9 cells, we found that Th9 related genes were greatly increased in IL-7 Th9 group, which demonstrated an enhanced Th9 differentiation. In CD4+ T cells, we found that IL-7 treatment resulted in a global gene expression change especially on chromatin remodeling related genes, which facilitated the entry of transcriptional factor to the Il9 promoter region and promoted Il9 transcription.

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Transcriptome analysis of TH2 CD4(+) T cells differentiated from wild-type and NLRP3KO mice.

Project description:The Nod-like receptor NLRP3 is involved in the formation of NLRP3. Up to now, the immunological functions of NLRP3 independently of inflammasome is unclear. In this dataset containing 6 samples (TH0, TH2 cells at day 3 and day 6 in wild type or Nlrp3 deficient cells), we show that NLRP3 expression in CD4(+) T cells supports a T helper 2 (TH2) transcriptional program in a cell-intrinsic manner (raw and normalized data are accessible on Gene Expression Omnibus database under the number GSE54561, http://www.dtd.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54561). Indeed, NLRP3 positively-regulated TH2 program independently of inflammasome formation. These data indicated that TH2 specific genes such as cMaf or Il4 were not induced in Nlrp3 deficient cells. These results demonstrate the capacity of NLRP3 to act as a key transcription factor in TH2 differentiation.

| S-EPMC4583695 | biostudies-literature

SIRT1 negatively regulates the differentiation of IL-9-producing CD4+T cells

Project description:Distinct metabolic programs support the differentiation of CD4+T cells into their separate lineages. In this study, we investigated metabolic mechanisms underlying the differentiation of IL-9 producing-CD4+T cells (TH9) in allergic airway inflammation and cancerous tumors. We found here that SIRT1 negatively regulates TH9 differentiation. A deficiency of SIRT1 induced by either conditional deletion in mouse CD4+T cells or the use of small interfering RNA (siRNA) in mouse or human T cells increased IL-9 production, whereas ectopic SIRT1 expression inhibited it. Notably, SIRT1-inhibited the differentiation of TH9 cells that regulated anti-tumor immunity and allergic pulmonary inflammation. Glycolytic activation through the mTOR-hypoxia-inducible factor-1Î± (HIF1Î±) pathway was required for the differentiation of the TH9 cells that confer protection against tumors and are involved in allergic airway inflammation. Our results define the essential features of a SIRT1-mTOR-HIF1Î± signaling-coupled glycolytic pathway in inducing TH9 cell differentiation, with implications for metabolic reprogramming as an immunotherapeutic approach. Lymphocytes were isolated from the spleen and lymph nodes of mice and sorted on a FACSAria II (Becton Dickinson). The sorted naÃ¯ve T cells (CD4+TCR+CD62Lhi CD44lo) from WT or SIRT1flox/flox-CD4-Cre mice were used for in vitro culture. T cells were activated with 2 ug/ml anti-CD3 (2C11; Bio X Cell), 2 ug/ml anti-CD28 (37.51; Bio X Cell) and 100 U/ml human IL-2. For TH9 cell differentiation, cultures were supplemented with 10 ng/ml IL-4 (R&D system), 2 ng/ml TGFÎ²1 (R&D system). After 5-6 d culture, differentiated T cells were collected and for microarray assay.

2016-06-14 | E-GEOD-79607 | biostudies-arrayexpress

SIRT1 negatively regulates the differentiation of IL-9-producing CD4+T cells

2016-06-14 | GSE79607 | GEO

Monocyte Subsets with High Osteoclastogenic Potential and Their Epigenetic Regulation Orchestrated by IRF8 [RNA-Seq sorted cells]

Project description:Currently, it is unclear if all monocyte subsets exhibit osteoclastogenic potential. Furthermore, the role of lineage determining TFs in regulating OC differentiation on a genome-wide scale remains poorly understood. In this study, we utilized a novel Irf8 conditional knockout (Irf8 cKO) mouse model to characterize the importance of IRF8 in OC progenitor development and epigenetic regulation of OC differentiation. To identify global transcriptional program governing the osteoclastogenic potential of Ly6Chi, Ly6Cint, and Ly6C– monocytes, and how it may be further influenced by IRF8 deficiency, we performed RNA-seq on sorted Ly6Chi, Ly6Cint, and Ly6C– cells from WT and Irf8 cKO mice. Cells were analyzed prior to (BMMs) and 4 days after RANKL stimulation (OCs). Here we show that WT Ly6Chi and Ly6Cint monocytes developmentally contain OC-specific transcripts, which are augmented upon RANKL stimulation. Additionally, in the absence of IRF8, OC-specific transcripts in all three monocyte subsets are primed to robustly respond to RANKL stimulation.

2020-09-11 | GSE151480 | GEO

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