Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type APC and OX40L-TG APC induced T helper 17 cell Transcriptomes [RNA-seq]

ABSTRACT: Purpose:The goals of this study are to evaluate the effect of OX40 ligation on transcriptome profiling of in vitro polarized T helper 17 cell (RNA-seq). Methods: mRNA profiles of CD4+ T cells cultured in vitro under Th17-polarizing conditions for 48hrs (both Ctrl and OX40L treated groups) were generated by deep sequencing, using Illumina RapidRun. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays Results: Among the 398 genes that were significantly affected by OX40, only about 11% were previously identified as RORγt target genes in Th17 cells. Conclusions: Our study suggests that OX40 unlikely affects Th17 commitment, but most likely impairs their effector differentiation. As IL-17A and IL-17F are Th17-defining cytokines, their suppression suggests that OX40 may inhibits effector functions of Th17 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE80010 | GEO | 2016/10/06

SECONDARY ACCESSION(S): PRJNA317660

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression

Project description:We examined the role of miR-155 in differentiated Th17 cells during their induction of Experimental Autoimmune Encephalomyelitis (EAE). Using adoptive transfer experiments, we found that highly purified, MOG antigen specific Th17 cells lacking miR-155 are defective in their capacity to cause EAE. Gene expression profiling of purified miR-155-/- IL-17F+ Th17 cells identified a subset of effector genes that are dependent upon miR-155 for their proper expression through a mechanism involving repression of the transcription factor Ets1. Among the genes reduced in the absence of miR-155 was IL-23R, resulting in miR-155-/- Th17 cells being hypo-responsive to IL-23. Taken together, our study demonstrates a critical role for miR-155 in Th17 cells as they unleash autoimmune inflammation, and finds that this occurs through a signaling network involving miR-155, Ets1 and the clinically relevant IL-23-IL-23R pathway. two biological replicates of miR-155-/- CD4+ IL-17F RFP+ T cells compared to two biological replicates of miR-155+/+CD4+IL-17F RFP+ T cells (as a control).

2013-05-01 | E-GEOD-45122 | biostudies-arrayexpress

OX40L protects against inflammation-driven fibrosis

Project description:Fibrosis is a leading cause of deaths in industrialized countries and has no effective therapy. We demonstrated that blockade of OX40L prevented inflammation-driven fibrosis affecting the skin and the lungs and promotes regression of established dermal fibrosis in different murine models. To characterize the pathways involved in the protection of skin fibrosis and affected by OX40L blocking, we used microarrays and identified distinct genes differentially expressed between ox40l+/+ and ox40l-/- in the bleomycin-induced dermal fibrosis mouse model. Total RNA were extracted from lesional skin samples of 3 ox40l+/+ and 4 ox40l-/- male mice aged 9 weeks treated with bleomycin for 3 weeks, and were hybridized on Affymetrix microarrays.

2016-08-09 | E-GEOD-73705 | biostudies-arrayexpress

Expression data from C57/Bl6 Wt mice CD4+ T cells after activation with anti-CD3 plus Wt APC or OX40L-Tg APC

Project description:OX40 is a T cell costimulatory molecule in the tumor necrosis factor receptor (TNFR) superfamily. Unlike other costimulatory molecules, OX40 is not expressed by naive T cells, but its expression is rapidly induced following T cell activation, and OX40 costimulation plays a critical role in cell survival, proliferation, and generation of memory cells. We used microarrays to detail the global programme of gene expression of activated CD4 T cells underlying OX40 costimulation and identified distinct classes of up-regulated genes after OX40 costimulation.

2018-05-15 | GSE104611 | GEO

OX40L protects against inflammation-driven fibrosis

2016-08-09 | GSE73705 | GEO

Tissue-restricted adaptive type-2 immunity is orchestrated by OX40L expression on group 2 innate lymphoid cells

Project description:We investigated the transcriptional profiles of lung ILC2, Th2 and Treg (Gata3+ and -) cells from naïve and IL-33-treated mice. This experiment accompanies our manuscript, where we showed that IL-33-dependent accumulation of adaptive type-2 immune cells (Th2 and Treg) was dependent on OX40L expression by ILC2.

2018-06-12 | GSE112937 | GEO

MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression

2013-05-01 | GSE45122 | GEO

IL-17 cytokines preferentially act on naïve CD4+ T cells

Project description:CD4+ Th17 T cells are a key helper population in the regulation of both protective immunity during infection and in self-tolerance. Through the secretion of IL-17, Th17 cells act in promotion of inflammation and thus a major therapeutic target for autoimmune disorders. Recent reports have brought to light that the IL-17 family cytokines, IL-17A, IL-17F and IL-17AF, can directly act on CD4+ T-cells, both in murine and human systems. Here we show that this action is preferentially targeted toward naïve, but not memory, CD4+ T-cells. Moreover, IL-17A, IL-17F and IL-17AF led to reduction in immune signaling genes, but an increase in interferon responsive genes across all treatments. In addition, IL-17A, IL-17F and IL-17AF treatment possessed differences in downstream transcriptional signaling, with IL-17AF heterodimer conferring both the greatest transcriptional change and suppressed phenotype. Detailed transcriptome analysis provides important functional insights into the genes and pathways that are modulated as a result of IL-17-mediated signaling.

2022-10-03 | GSE159406 | GEO

The cytokine IL-17A limits Th17 pathogenicity via a negative feedback loop driven by autocrine induction of IL-24

Project description:Dysregulated Th17 cell responses underlie multiple inflammatory and autoimmune diseases, including autoimmune uveitis and its animal model, EAU. However, clinical trials targeting IL-17A in uveitis were not successful. Here, we found that Th17 cells were regulated by their own signature cytokine, IL-17A. Loss of IL-17A in autopathogenic Th17 cells did not reduce their pathogenicity and instead elevated their expression of the Th17 cell cytokines GM-CSF and IL-17F. Mechanistic in vitro studies revealed a Th17 cell-intrinsic autocrine loop triggered by binding of IL-17A to its receptor, leading to activation of transcription factor NFκB and induction of IL 24, which repressed the Th17 cytokine program. In vivo, IL-24 treatment ameliorated Th17-induced EAU, whereas silencing of IL-24 in Th17 cells enhanced disease. This regulatory pathway also operated in human Th17 cells. Thus, IL-17A limits pathogenicity of Th17 cells by inducing IL-24. These findings may explain the disappointing therapeutic effect in targeting IL-17A in uveitis.

2020-07-22 | GSE152534 | GEO

Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (RNA-Seq)

Project description:Th17 cells secrete IL-17A, IL-17F, IL-21, and IL-22 cytokines that are critical in mediating inflammation and protecting the host from microorganisms infection. The basic leucine zipper transcription factor ATF-like (Batf) contributes to the transcriptional programming of multiple effector T cells, and is required for Th17 cell development. Here, we have interrogated mechanisms by which Batf promotes and stabilizes Th17 cell phenotype. We have shown that in vitro differentiated Th17 cells have increased expression of Th1 and Treg signature genes in the absence of Batf. In addition, Citrobacter rodentium infected Batf-deficient (Batf KO) mice fail to clear the infection, and that is correlated with diminished IL-17A and IL-22 cytokine production and increased Foxp3 and Ifng expression compared to WT mice. We find that Batf sustains Th17 phenotype in long-term culture conditions by suppressing Th1- and Treg-specific gene expression. Mechanistically, we reveal that Batf negatively regulates IL-2-STAT5 signaling and modulates STAT5 binding at the Ifng and Foxp3 gene loci thus suppressing Th1-Treg phenotype in Th17 cell development. Inhibition of STAT5 DNA binding activity in Batf KO Th17 cells was able to repress Ifng and Foxp3 expression compared to control-treated cells. Moreover, STAT5 cooperates with transcription factors Ets1 and Runx1 to mediate epigenetic modification and regulate gene expression. Thus, our study has revealed an essential function of Batf in modulating the IL-2-STAT5 signaling to promote and stabilize Th17 cell development.

2023-04-26 | GSE167418 | GEO

Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (ChIP-Seq)

2023-04-26 | GSE167417 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data