CD4+ T cells have different gene profiles between Ogt-KD and control mice after EAE
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ABSTRACT:
PROVIDER: PRJNA640528 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12053477_1.fastq.gz | Fastqsanger.gz | |||
| SRR12053477_2.fastq.gz | Fastqsanger.gz | |||
| SRR12053478_1.fastq.gz | Fastqsanger.gz | |||
| SRR12053478_2.fastq.gz | Fastqsanger.gz | |||
| SRR12053479_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate whether the level of O-GlcNAc could affect CD4+ T cell function after EAE, we performed RNA-sequencing analysis on splenic CD4+ T cells. The downregulation of OGT in CD4+ T cells led to changes in gene expression profile in CD4+ T cells with a 2-fold threshold. Next, Gene Ontology (GO) analysis was performed to compare differentially expressed genes in Ogt-KD and control mice. These results indicated that OGT was involved in the regulation of multiple important cellular events.
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Project description:EAE is a mouse model of human multiple sclerosis. We used miRNA low density array to screen abnormally expressed miRNAs in autoimmune CD4+T cells.Generally, splenic CD4+T cells were isolated from three groups: healthy C57BL/6 mice, C57BL/6 mice with the induction of EAE for 16 days, and C57BL/6 mice with the induction of EAE for 32 days. Then we did miRNA profilings on these samples. Splenic CD4+T cells were isolated from the above three groups. Each group consist of six mice. Equal amount total RNA from each mouse was pooled prior to miRNA expression analysis.
2015-05-08 | E-GEOD-66621 | biostudies-arrayexpress
Project description:EAE is a mouse model of human multiple sclerosis. We used miRNA low density array to screen abnormally expressed miRNAs in autoimmune CD4+T cells.Generally, splenic CD4+T cells were isolated from three groups: healthy C57BL/6 mice, C57BL/6 mice with the induction of EAE for 16 days, and C57BL/6 mice with the induction of EAE for 32 days. Then we did miRNA profilings on these samples.
2015-05-08 | GSE66621 | GEO
Project description:Purpose: To compare gene expression of CD4+ T cells between Type-A and Type-B EAE Method: CD4+ T cells were FACS sorted from spleens 9-day post immunization. Results: We found that Type-B EAE (NLRP3 inflammasome-dependent and IFNb treatment-resistant EAE) express high levels of CXCR2 and other chemokine receptors, which can be targeted to treat the Type-A EAE subtypes, instead of treating with IFNb. Conclusions: Altering intensity of immunization significantly impacts on gene expression patterns in T cells.
2016-11-07 | GSE85946 | GEO
Project description:TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. Evidence has linked TET1 function to epigenetic repression complexes, yet mechanistic information, especially for the TET2 and TET3 proteins, remains limited. Here, we show a direct interaction of TET2 and TET3 with O-GlcNAc transferase (OGT). OGT does not appear to influence hmC activity, rather TET2 and TET3 promote OGT activity. TET2/3-OGT co-localize on chromatin at active promoters enriched for H3K4me3 and reduction of either TET2/3 or OGT activity results in a direct decrease in H3K4me3 and concomitant decreased transcription. Further, we show that Host Cell Factor 1 (HCF1), a component of the H3K4 methyltransferase SET1/COMPASS complex, is a specific GlcNAcylation target of TET2/3-OGT, and modification of HCF1 is important for the integrity of SET1/COMPASS. Additionally, we find both TET proteins and OGT activity promote binding of the SET1/COMPASS H3K4 methyltransferase, SETD1A, to chromatin. Finally, studies in Tet2 knockout mouse bone marrow tissue extend and support the data as decreases are observed of global GlcNAcylation and also of H3K4me3, notably at several key regulators of haematopoiesis. Together, our results unveil a step-wise model, involving TET-OGT interactions, promotion of GlcNAcylation, and influence on H3K4me3 via SET1/COMPASS, highlighting a novel means by which TETs may induce transcriptional activation. ChIP-Seq experiments were performed on Illumina HiScanSQ sequencer in wild-type HEK293T cells for H3K4me3 histone marks, O-GlcNAc and HCF1, for HT-TET2, HT-TET3 and HT-OGT in HEK293T cells overexpressing those three fusion proteins and in TET2 Kd HEK293T cells for H3K4me3 histone marks. ChIP-Seqs were also performed in mouse bone marrow tissues for H3K4me3 histone marks, O-GlcNAc, endogenous Tet2 and in Tet2 Ko bone marrow tissues for H3K4me3 histone marks.
2013-02-07 | E-GEOD-36620 | biostudies-arrayexpress
Project description:TET2 directly interacts with OGT, which is important for the chromatin association of OGT in vivo. Although this specific interaction does not regulate the enzymatic activity of TET2, it facilitates OGT-dependent histone O-GlcNAcylation. Moreover, OGT associates with TET2 at transcription starting sites (TSS). Down-regulation of TET2 reduces the amount of H2B S112 GlcNAc marks in vivo, which are associated with gene transcription regulation. We found that OGT interacts with TET2 tightly. Using ChIP-seq with specific antibodies, we tested the co-localization of TET2 and OGT in genome level.
2012-12-11 | E-GEOD-41720 | biostudies-arrayexpress
Project description:Experimental autoimmune encephalomyelitis (EAE) is a murine model of multiple sclerosis, a chronic neurodegenerative and inflammatory autoimmune condition of the central nervous system (CNS). Pathology is driven by the infiltration of autoreactive CD4+ lymphocytes into the CNS where they attack neuronal sheaths causing ascending paralysis. We used an isotope-coded protein labelling approach to investigate the proteome of CD4+ cells isolated from the spinal cord and brain of mice at various stages of EAE progression in two EAE disease models; PLP139-151-induced relapsing-remitting EAE and MOG35-55-induced chronic EAE, which emulate the two forms of human multiple sclerosis. A total of 1120 proteins were quantified across disease onset, peak-disease and remission phases of disease and of these, 13 up-regulated proteins of interest were identified with functions relating to the regulation of inflammation, leukocyte adhesion and migration, tissue repair and the regulation of transcription/translation. Proteins implicated in processes such as inflammation (S100A4 and S100A9) and tissue repair (Annexin A1), which represent key events during EAE progression were validated by quantitative PCR. This is the first targeted analysis of autoreactive cells purified from the CNS during EAE, highlighting fundamental CD4+ cell-driven processes that occur during the initiation of relapse and remission stages of disease.
2016-07-08 | PXD001011 | Pride
Project description:Purpose: To elucidate the potential immune-regulatory mechanism of TRAIL of activated T cells in EAE, we analyzed gene expression profiles of splenic CD4+ T cells from EAE mice treated with TRAIL by RNA sequencing and transcriptome analysis. Methods: Splenic CD4+ T cell mRNA profiles of control or EAE mice treated with vehicle or TRAIL were generated by deep sequencing using Illumina Solexa. Library construction of all samples were used by Agilent's SureSelect Strand Specific RNA Library Preparation Kit for 75SE (Single-End or Paired-End) sequencing on Solexa platform. The sequence was directly determined using sequencing-by-synthesis technology via the TruSeq SBS Kit. Raw sequences were obtained from the Illumina Pipeline software bcl2fastq v2.0 and expected to generate 20M (million reads or Gb) per sample. Results: By comparing mRNA exression of splenic CD4+ T cells from EAE mice treated with vehicle or TRAIL, there were 244 genes significantly differentially expressed. By analyzing these 244 significant genes categorized by a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the most significantly enriched category for CD4+ T cells was “cell cycle” (multiple of enrichment: 3.13, p = 1.64 × 10−5) followed by “TCR signaling pathway” (multiple of enrichment: 2.80, p = 8.25 × 10−4). In addition, significant genes in the“TCR signaling pathway” tended to be downregulated while those in “cell cycle”tended to be upregulated in a volcano plot analysis. Consistent with the volcano plot results, by using unsupervised hierarchical clustering, the heatmap showed that significant TCR signaling pathway-associated genes were downregulated, while significant cell cycle-associated genes were upregulated in splenic CD4+ T cells from EAE mice treated with TRAIL Conclusions: Our study demonstrated the gene transcription pattern from CD4+ T cells of TRAIL-treated EAE mice were involved in distinct TCR signaling and cell cycle pathways.
2017-12-27 | GSE108523 | GEO
Project description:Protein arginine methyltransferase 5 (Prmt5) is the major type II methyltransferase catalyzing symmetric dimethylation, regulates cell development, homeostatic and disease processes. Prmt5 inhibition or deletion in CD4+T cells has been reported to protection against experimental autoimmune encephalomyelitis (EAE), the perfect mouse model for multiple sclerosis (MS); however, the detail mechanisms have not yet been elucidated. Here, using the mRNA sequencing, single cell RNA sequencing and ATAC sequencing, we uncovered the unreported role of Prmt5 on T cells migration ability under the EAE condition. We found that mice condition knockout of Prmt5 in T cells were resistance with EAE, infiltrating inflammatory CD4+ T cells in center nervous system (CNS) were greatly reduced. However, T cells in spleen showed much more proliferation and activation properties in Prmt5cko mice, the number of pathogenic CD4+T cells in spleen were not reduced. We further revealed that Rora+CD4+T cells were elevated in Prmt5cko mice, but expressed lower level of S1pr1, resulting in a lack of CD4+ T cells egress from spleen and migrate to CNS, leading to pathogenic CD4+T cells were blocked in spleen. Moreover, single cell ATAC sequencing revealed that Klf2 were enriched in S1pr1 promoter and reduced in Prmt5cko mice. Correctively, our study delineated the undiscovered role of Prmt5 on T cell biology, Prmt5 may through Klf2-S1pr1 pathway and regulate T cells migration; modulating Prmt5 levels may be useful for controlling CD4+T cell migration in CD4+T cell mediated diseases including MS.
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