Chromatin accessibility timecourse of Naïve to Th17 polarization in wildtype mouse CD4 T cells [ATAC-seq]
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PROVIDER: PRJNA661772 | ENA |
REPOSITORIES: ENA
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Project description:We applied ATACseq technology for mapping chromatin accessibility during CD4+ T cells activation. Briefly, we generated genome-wide chromatin-state maps of naive, Th17 at 48 hours and 72 hours. Using a series of ATAC-seq timecourse experiment, we revealed that chromatin accessibility is dynamic between naive and Th17, especially at the Th17 singature gene loci. These open chromatin sites may function as important cis-regulate elements for cell-specific genes expression.
2024-12-31 | GSE157576 | GEO
Project description:Gene expression in naïve and Th17 cell were characterized. We report a notable dynamic change in the expression of genes encoding RNA editing enzymes. Birefly, the transcript encoding ADAR2 (Adarb1) was significantly upregulated in Th17 cells, and the transcript encoding ADAR1 (Adar) was downregulated during the polarization from naive to Th17 cells. The altered expression of RNA editing genes results in the dynamic A-to-I editing in naive and Th17 cells. In addtion, loss of DDX5 dysregulated ADAR2 expression, resulting in altered A-to-I editing on a subset of Th17 transcripts.
2024-12-31 | GSE157578 | GEO
Project description:GRID-seq studies of mouse naïve and culture Th17 cells from wildtype mice
| PRJNA787543 | ENA
Project description:Analysis of Th17 polarization under different oxygen concentrations and environmental toxin exposure at gene expression level. Results provide important information of the response of CD4+ T cells to low oxygen , such as genes involved in metabolism, transcriptional factor, up- or down-regulated specific cellular functions.
2017-06-01 | GSE90882 | GEO
Project description:Transcriptomic studies of mouse naïve and Th17 cell from wildtype or Malat1 deficient background
| PRJNA787542 | ENA
Project description:IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. Gene array analysis on Stat6 and T-bet double deficient Th17 cells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TGFbeta, and associated with Th17 IL-10 production. Both c-Maf and IL-10 induction during Th17 polarization depended on Stat3, but not Stat6 or Stat1, and mechanistically differed from IL-10 regulation by Th2 or IL-27 signals. TGFbeta was also synergistic with IL-27 to induce c-Maf, and induced Stat1 independent IL-10 expression in contrast to IL-27 alone. Retroviral transduction of c-Maf was able to induce IL-10 expression in Stat6 deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression through binding to a MARE motif in the IL-10 promoter. Together, these data reveal a novel role for c-Maf in regulating T effector development, and suggest that TGFbeta may antagonize Th17 immunity by IL-10 production through c-Maf induction. Our recent studies showed that IL-6 combined with TGFbeta differed from IL-6 combined with IL-23 for IL-10 production and pathogenic activities in CD4 T cells deficient in Stat6 and T-bet, despite similar IL-17 production. We performed gene array analysis on Stat6 and T-bet double deficient cells. We rationalized that by comparing gene expression in cells treated with IL-6 plus TGFbeta versus TGFbeta alone, we would be able to identify genes specific for standard Th17 polarization, and responsible for both IL-17 and IL-10 expression. By next comparing gene expression in cells treated with IL-6 plus TGFbeta versus IL-6 plus IL-23, we could eliminate molecules involved solely in IL-17 regulation, and obtain genes specifically responsible for IL-10 regulation.
2009-03-03 | E-GEOD-15029 | biostudies-arrayexpress
Project description:Transcriptomic studies of mouse naïve and Th17 cell from wildtype or DDX5 deficient background [RNA-seq]
| PRJNA661773 | ENA
Project description:Epigenetic mechanisms contribute to shaping many aspects of adaptive immunity, including T cell lineage functions in anti-infective surveillance. Histone deacetylases (HDAC) control T cell polarization but a role in fungal-specific T cell responses remains poorly understood. Here we show that CD4+ T cells are an integral part of the adaptive immune defense against invasive fungal infections. Temporally-resolved in vivo transcriptional profiles of splenic Th cells from infected mice harboring a CD4+-specific ablation of HDAC1 reveals its critical role in limiting T cell polarization towards Th17 at the expense of Th1-lineage commitment. Mechanistically, HDAC1 restricts expression of the cytokine receptors gp130 and TGFbRII on the T cell surface thus limiting Stat3 and Smad2/3 signaling in a fungal-specific manner. Controlled release of Th17-associated cytokines IL-17A and GM-CSF is vital to minimize epithelial apoptotic processes in renal tubular epithelial cells (RTECs) in vitro as well as during systemic infections in vivo. Consequently, protecting the host from excessive organ pathology, loss of kidney functionality and limiting fungal burdens, thus reducing sepsis-induced death during fungal infections. Collectively, this work shows that HDAC1 controls T cell lineage polarization, thus playing a critical role in the antifungal immune defense and infection outcome.
2024-12-05 | GSE271923 | GEO
Project description:There remains a need for analysis of CD4 helper T cells differentiation in vivo. To this end ovalbumin (OVA)-specific CD4 (OTII) T cells transferred into congenic mice were studied. Live attenuated OVA-expressing Salmonella (SalOVA) induce T-bet and IFN-g in OTII cells, while alum-precipitated OVA (alumOVA) induces GATA-3 and IL-4. Although 70% of alumOVA-responding OTII cells express GATA-3, only 7% produce IL-4. Thus Th2-polarization defined solely by IL-4 production does not recognize the diversity of GATA-3-expressing effectors. Low-density arrays were designed to assess the expression of 384 genes by real-time RT-PCR. Extensive early diversification occurred in both responses. SalOVA selectively induced many chemokines and pro-inflammatory cytokines, while alumOVA induced few Th2-associated cytokines. Several cytokines and molecules associated with Th17 cells and follicular helper cells were also induced by both antigens. The transcription factor Helios was exclusively induced in alumOVA-responding OTII cells, and critically not in standard in vitro Th2-polarization systems. Early synchronous up-regulation of Helios and GATA-3 mRNA is paralleled at protein level with largely coincident localization in specific nuclear foci of OTII cells responding to alumOVA. This appears to be consistent with a key role for both transcription regulators in the direction of Th2 responses in vivo. Keywords: In vivo T cell polarization Ovalbumin (OVA)-specific CD4 (OTII) T cells were transferred into C57BL/6 mice that were immunized either with live attenuated OVA-expressing Salmonella (Sal) or with alum-precipitated OVA (alum), or not (Naïve). Gene expression assay was performed on FACS sorted OTII cells (Naïve, Sal, Alum). OTII cells were purified from three independent groups of ten naïve, or SalOVA-immunized or alumOVA-immunized mice.
2008-06-27 | E-GEOD-7481 | biostudies-arrayexpress
Project description:Long non-coding RNAs (lncRNAs) are critical regulators of mammalian gene programs. Metastasis Associated Lung Adenocarcinoma Transcript 1 (Malat1) is the most abundant lncRNA expressed in intestinal Th17 cells critical for maintaining tissue homeostasis and regulating local inflammation. Here, we report that Malat1 negatively regulates IL-17A and IL-17F productions in intestinal Th17 cells during colitis and contributes to local inflammation. Global RNA interactions with DNA by deep sequencing (GRID-seq) coupled with transcriptomic studies revealed Malat1 is recruited to the Il17a-Il17f super enhancer in Th17 cells, and regulates Il17a-Il17f transcription.
2024-12-31 | GSE190560 | GEO