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Overexpression of RORA in primary mouse in vitro Th2

ABSTRACT: Overexpression of RORA in primary mouse in vitro Th2

PROVIDER: PRJEB32840 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3348140_1.fastq.gz	Fastqsanger.gz
	ERR3348140_2.fastq.gz	Fastqsanger.gz
	ERR3348150_1.fastq.gz	Fastqsanger.gz
	ERR3348150_2.fastq.gz	Fastqsanger.gz
	ERR3348160_1.fastq.gz	Fastqsanger.gz

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Overexpression of RORA in primary mouse in vitro Th2

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

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Overexpression of spliced XBP1 in in vitro Th2 cells, and comparison to 4u8c treatment

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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.

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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.

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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.

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Transcriptomic analysis of WT versus Ikzf4-/- CD4+ T cells cultured in Th2-polarizing conditions

Project description:The Ikaros zinc finger transcription factor Eos has been commonly implicated in regulatory T cells to promote their immunosuppressive functions. Paradoxically, a new role is emerging for Eos in promoting pro-inflammatory responses of conventional CD4+ T cells in the dysregulated setting of autoimmunity. Even so, the precise role of Eos in regulating the differentiation and function of healthy effector CD4+ T cell subsets remains unclear. Here, we find that Eos is a positive regulator of CD4+ T helper 2 (TH2) cells—effector T cells implicated in the induction of allergic asthma. Using murine in vitro TH2 cells and an in vivo house dust mite asthma model, we found that Eos-deficient T cells had reduced expression of key TH2 transcription factors, effector cytokines, and differentiation receptors. Mechanistically, among various TH2-polarizing pathways, the IL-2/STAT5 axis and its downstream TH2 gene targets emerged as one of the most significantly downregulated networks in Eos deficiency. Using in vitro TH2 cells and overexpression of Eos zinc-finger-domain mutants, we discovered that Eos forms a novel complex with and supports the tyrosine-phosphorylated signaling activity of STAT5. Overall, these data define a novel regulatory mechanism whereby Eos promotes IL-2/STAT5 activity to facilitate TH2 differentiation.

2023-02-01 | GSE216737 | GEO

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