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RORA proximal enhancer regulates its expression during early human Th17 cell differentiation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE243064 | GEO | 2024/05/23

REPOSITORIES: GEO

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RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ChIP]

Project description:Distal regulatory elements, such as enhancers, play a pivotal role in dictating cell identity by controlling the transcriptional status of specific cells. The comprehensive understanding of the epigenetic landscape, encompassing enhancer establishment and chromatin accessibility, during the differentiation of human Th17 cells remains incomplete. Leveraging ATAC-seq based chromatin accessibility profile along with the profiling of key histone marks we identified potential enhancers crucial for fate specification of Th17 cells. We found that 24 single nucleotide polymorphisms (SNPs) associated with autoimmune diseases were located near Th17-enhancers. Interestingly, these SNPs overlapped the binding sites of transcription factor active in Th17 cells. Among the Th17 specific enhancers, we identified an enhancer in the intron of RAR-related orphan receptor alpha (RORA) that was earlier predicted to regulate RORA expression. Functional validation through luciferase reporter assays confirmed that this enhancer positively regulate the transcription. Moreover, employing CRISPR-Cas9-mediated deletion of a transcription factor binding site-rich region within the identified RORA enhancer, we demonstrated its role in regulating RORA transcription. These findings provide insights into the potential mechanism by which the RORA enhancer modulates Th17 differentiation and into the role of regulatory SNPs within noncoding regions in conferring resistance or susceptibility to Th17 cell-mediated autoimmune pathologies.

2024-05-23 | GSE243062 | GEO

RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ATAC]

2024-05-23 | GSE243058 | GEO

RORA proximal enhancer regulates its expression during early human Th17 cell differentiation

Project description:RORA proximal enhancer regulates its expression during early human Th17 cell differentiation

| PRJNA1016309 | ENA

RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ChIP]

Project description:RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ChIP]

| PRJNA1016307 | ENA

RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ATAC]

Project description:RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ATAC]

| PRJNA1016305 | ENA

Cyclooxygenase-2 regulates Th17 cell differentiation during allergic lung inflammation.

Project description:RationaleTh17 cells comprise a distinct lineage of proinflammatory T helper cells that are major contributors to allergic responses. It is unknown whether cyclooxygenase (COX)-derived eicosanoids regulate Th17 cells during allergic lung inflammation.ObjectivesTo determine the role of COX metabolites in regulating Th17 cell differentiation and function during allergic lung inflammation.MethodsCOX-1(-/-), COX-2(-/-), and wild-type mice were studied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of Th17 differentiation using flow cytometry, cytokine assays, confocal microscopy, real-time polymerase chain reaction, and immunoblotting. In addition, the role of specific eicosanoids and their receptors was examined using synthetic prostaglandins (PGs), selective inhibitors, and siRNA knockdown.Measurements and main resultsTh17 cell differentiation in lung, lymph nodes, and bronchoalveolar lavage fluid was significantly lower in COX-2(-/-) mice after ovalbumin sensitization and exposure in vivo. In vitro studies revealed significantly impaired Th17 cell differentiation of COX-2(-/-) naive CD4(+) T cells with decreased Stat3 phosphorylation and RORγt expression. Synthetic PGF(2α) and PGI(2) enhanced Th17 cell differentiation of COX-2(-/-) CD4(+) T cells in vitro. The selective COX-2 inhibitor, NS-398, and PGF(2α) receptor and PGI(2) receptor siRNA knockdown significantly decreased Th17 cell differentiation in vitro. Administration of synthetic PGs restored accumulation of Th17 cells in lungs of allergic COX-2(-/-) mice in vivo.ConclusionsCOX-2 is a critical regulator of Th17 cell differentiation during allergic lung inflammation via autocrine signaling of PGI(2) and PGF(2α) through their respective cell surface receptors.

| S-EPMC3172888 | biostudies-literature

Gcn5 regulates FGF signaling outputs through c-Myc during early differentiation of embryoid bodies

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-12-14 | GSE104454 | GEO

H3K4 mono- and di-methyltransferase MLL4 is required for enhancer activation during cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-12-17 | E-GEOD-50466 | biostudies-arrayexpress

Rexinoid signalling during early myogenic differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-09-13 | GSE94561 | GEO

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

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