Overexpression of RORA in primary mouse in vitro Th2
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ABSTRACT:
PROVIDER: PRJEB32840 | ENA |
REPOSITORIES: ENA
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Project description:Naive CD4 T cells were taken from spleens of wild-type mice, and activated with CD3/CD28. IL4 was added to induce Th2. The cells were transduced with retrovirus to overexpress RORA vs control. Three different viral constructs were tested. M6-Rora2_mCherry appear to give the best result based on RNAseq validation of Rora expression. Rora2 = ENSMUST00000113624
2019-06-10 | E-MTAB-8001 | biostudies-arrayexpress
Project description:In this expriment, Nave T cells were isolated from both RORA knockout mice and wild type mice and were differentiated towards Th2. RNA was isulated from those cells 4 days after, to identify genes that might be regulated by RORA.This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2015-11-03 | E-ERAD-411 | biostudies-arrayexpress
Project description:This experiment shows that the in vitro effect of 4u8c on Th2 cells can be rescued using XBP1s overexpression
2018-10-06 | E-MTAB-7104 | biostudies-arrayexpress
Project description:Overexpression of spliced XBP1 in in vitro Th2 cells, and comparison to 4u8c treatment
| PRJEB28078 | ENA
Project description:The retinoic acid receptor-related orphan receptor a (RORa) is a member of the NR1 subfamily of orphan nuclear hormone receptors. RORa is an important regulator of various biological processes, including cerebellum development, cancer and circadian rhythm. To determine molecular mechanism by which hepatic deletion of RORa induces obesity and insulin resistance, we performed global transcriptome analysis from high-fat diet (HFD)-fed RORa f/f and RORa LKO mouse liver tissues. This analysis provides insight into molecular mechanisms for RORa in high-fat-diet condition.
2017-06-28 | GSE83338 | GEO
Project description:To test whether human in vitro primed Th9 cells recapitulate the core pathogenic Th2 cell phenotype, we differentiated naïve T cells into Th1 (IL-12), Th2 (IL-4), Th9 (IL-4+TGF-β), and iTreg (TGF-β). After 7 days transcriptomic profiling by bulk RNA-seq was performed.
2022-10-31 | E-MTAB-12199 | biostudies-arrayexpress
Project description:We performed RNAseq to identify mRNAs that were specifically down regulated in neutrophils when RORa function is inhibited
2021-04-06 | GSE171501 | GEO
Project description:Full development of IL-17 producing CD4+ T helper cells (TH17 cells) requires the transcriptional activity of both orphan nuclear receptors RORa and RORgt. Despite this evidence, RORa is considered functionally redundant to RORgt; thus, the function and therapeutic value of RORa in TH17 cells remains underexplored. Using mouse models of autoimmune and chronic inflammation, we show that expression of RORa is required for TH17 cell pathogenicity. T-cell specific deletion of RORa reduced the development of experimental autoimmune encephalomyelitis (EAE) and colitis. Reduced inflammation was associated with decreased TH17 cell development, lower expression of tissue-homing chemokine receptors and integrins, and increased frequencies of Foxp3+ T regulatory (Treg) cells. Importantly, inhibition of RORa with a selective small molecule antagonist largely phenocopied our genetic data, potently suppressing the in vivo development of both chronic/progressive and relapsing/remitting EAE but had no effect on overall thymic cellularity. Furthermore, use of the RORa antagonist effectively inhibited human TH17 cell differentiation and memory cytokine secretion. Together, these data suggest that RORa acts independently of RORgt in programming TH17 pathogenicity and identifies RORa as a safer and more selective therapeutic target for the treatment of TH17-mediated autoimmunity.
2020-10-29 | GSE160327 | GEO
Project description:Host defense against diverse pathogens involves the recruitment and differentiation of CD4+ T effector subsets including T helper 1 (Th1), Th2, Th17 and induced regulatory T (Treg) cells. Surface phenotype studies have revealed subset-specific surface markers for the identification and purification of human primary CD4+ T effector subsets. In the present study, we aimed to characterize the mRNA and large intergenic non-coding RNA (lincRNA) expression differences between human primary CD4+ T effector subsets and identify potential subset-specific genes. To achieve this goal, mRNA and lincRNA microarray profiling of flow cytometry-sorted human primary Th1, Th2, Th17 and Treg cells was performed. Principal component and pathway analyses revealed subset-specific gene expression patterns. A Th2-specific lincRNA, GATA3-AS1, also termed FLJ45983, was identified in primary immune cells and tissues, as well as in in vitro polarized CD4+ T effector subsets. Further analysis showed that GATA3-AS1 was a potential diagnostic marker in allergy, a Th2-associated disease. This first systematic genome-wide analysis of gene expression differences between primary CD4+ T effector subsets may help to identify novel regulatory protein-coding genes and lincRNAs regulating CD4+ T cell subset differentiation, as well as potential diagnostic markers. As an example, we identified a GATA3-associated Th2-specific marker lincRNA GATA3-AS1. Gene expression microarray analysis of flow-cytometry sorted human primary naïve CD4+ T cells, CD4+ T central memory cells, Th1, Th2, Th17 and Treg cells from buffy coat of four healthy controls Gene expression microarray analysis was performed using SurePrint G3 Human Gene Expression 8X60K microarray.
2013-06-01 | E-GEOD-43005 | biostudies-arrayexpress
Project description:RORasg/sg mice have small cardiomyocytes and hypocontractile hearts with increased fibrosis. Microarrays revealed broad deficits of sarcomeric RNAs and key myogenic transcription factors, suggesting that the loss of RORa leads to impaired developmental hypertrophy through transcriptional regulation. RORasg/sg mice developed exaggerated ventricular remodeling in response to Agn II infusion. We identify novel cardioprotective roles for RORa in promoting developmental and preventing pathological cardiac hypertrophy, mediated in part through regulation of the IL-6-STAT3 pathway in cardiomyocytes and cardiac fibrosis
2021-04-12 | GSE98892 | GEO