Anti-CD3 model of intestinal inflammation
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB85305 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR14221600_1.fastq.gz | Fastqsanger.gz | |||
| ERR14221600_2.fastq.gz | Fastqsanger.gz | |||
| ERR14221601_1.fastq.gz | Fastqsanger.gz | |||
| ERR14221601_2.fastq.gz | Fastqsanger.gz | |||
| ERR14221602_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Engagement of the ICOS receptor represents a key event in a process that culminates in Bcl6 expression and acquisition of the TFH and TFR phenotype. To better understand the essentials of ICOS-mediated signaling pathway, we profiled the changes in gene expression elicited after co-ligation of ICOS and CD3 compared with CD3 ligation alone. Naïve CD4+ T-cells were purified from single cell suspensions of B6 spleen and stimulated with anti-CD3 and anti-CD28 for 2d followed by resting overnight before 20 min of incubation with anti-CD3 and/or anti-ICOS and cross-linking with goat anti-hamster Ab for 8h. RNA was prepared, amplified, labeled and hybridized to Mouse Gene 1.0 ST Array (Affymetrix), in quadruplicates for anti-CD3 ligation and duplicates for anti-CD3/ anti-ICOS co-ligation.
2014-09-23 | E-GEOD-61284 | biostudies-arrayexpress
Project description:Type 1 diabetes (T1D) results from autoimmune destruction of β cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas of diabetic NOD mice treated with anti-CD3 mAb and IL-1RA combination therapy. The treatment reversed hyperglycemia compared to the anti-CD3 alone control group. We observed enhanced expression of PTPN2, a T1D candidate gene, and endoplasmic reticulum (ER) chaperones in the islets from cured mice.
2022-11-10 | PXD025394 | Pride
Project description:KY1044 is a human monoclonal IgG1 that selectively binds to Inducible T cell CO-stimulator (ICOS). The co-stimulatory effect of KY1044-stimulated human T cells was analysed by RNA sequencing (RNA seq). Purified pre-activated (ICOS+ve) T cells were stimulated with either KY1044 and anti-CD3 or anti-CD3 alone and cells were harvested for RNA seq after 6hrs. Kallisto transcript abundance are provided in the absence of raw sequence reads.
2020-09-01 | E-MTAB-9500 | biostudies-arrayexpress
Project description:Type 1 Diabetes (T1D) is a chronic autoimmune disease resulting from T cell-mediated destruction of pancreatic beta cells. Although T cells are known to destroy beta cells, how they may impact non-lethal forms of beta cell stress that also contribute to T1D development is not known. Here, we established an intermittent treatment regimen using a validated monoclonal anti-CD3 antibody on the female nonobese diabetic (NOD) mouse model for T1D at late prediabetic stages that leads to depletion of antigen-specific T cells and improvement of glucose tolerance. We used mRNA-seq to explore transcriptomic changes in isolated pancreatic islets from mice treated with anti-CD3 antibody or IgG as a control.
2025-06-13 | GSE275350 | GEO
Project description:The tolerogenic anti-CD3 monoclonal antibodies (anti-CD3) are promising compounds for the treatment of type 1 diabetes (T1D). Anti-CD3 administration induces transient T-cell depletion both in preclinical and in clinical studies. Notably, said depletion mainly affects CD4+ but not CD8+ T cells. Moreover, T1D reversal in preclinical models is accompanied by the selective expansion of CD4+FOXP3+ T regulatory (Treg) cells, which are fundamental for the long-term maintenance of anti-CD3-mediated tolerance. The mechanisms that lead to this immune-shaping by affecting mainly CD4+ T effector cells while sparing CD4+FOXP3+ Treg cells have still to be fully elucidated. This study shows that CD3 expression levels differ from one T-cell subset to another. CD4+FOXP3- T cells contain higher amounts of CD3 molecules than do CD4+FOXP3+ and CD8+ T cells both in mice and in humans. Said differences may explain the anti-CD3-mediated immune resetting that occurs in vivo after anti-CD3 administration in mice. In addition, transcriptome analysis demonstrates that CD4+FoxP3+ Treg cells are significantly less responsive than CD4+FoxP3- T cells to anti-CD3 treatment at molecular levels. Thus, heterogeneity in CD3 expression likely confers the various T-cell subsets differing susceptibility to in vivo tolerogenic anti-CD3-mediated modulation. This data sheds new light on the molecular mechanism that underlies anti-CD3-mediated immune resetting, and thus may open new opportunities to improve this promising treatment.
2015-01-19 | E-MTAB-2437 | biostudies-arrayexpress
Project description:PBMCs were isolated from whole blood taken from one patient and one healthy control. Cells were cultured in media (RPMI) alone, with 1µg/ml anti-CD3, with 1µg/ml anti-CD3 & 1µg/ml anti-CD28 or with 0.5ng/ml LPS. Cells were harvested after 24 or 48 hours, RNA isolated using Trizol, purified using RNeasy columns and labelled using Illumina TotalPrep RNA Amplificiation kit (Applied Biosystems) before hybridisation to Illumina HumanRef-8 arrays.
2022-04-01 | E-MTAB-101 | biostudies-arrayexpress
Project description:Proteomics analysis of a mouse model for intestinal inflammation (IBD) and Caco2 cells used as inflammation model.
2020-11-09 | PXD020245 | Pride
Project description:Purpose: The aim of this study is the evaluation of differential gene expression profile by RNA-seq in response to anti-CD3 treatment in CD3 cells obtained from blood samples of healthy donors, to achieve a better understanding of the antibodies molecular mechanisms of action. In this study T cells were treated in the complex PBMC milieu, in a tentative to mimetize the natural ambient that occurs in a clinical administration of therapeutic anti-CD3. Methods: Human peripheral blood mononuclear cells were purified from healthy volunteers blood and were cultured in the presence of the monoclonal antibody OKT3 or a recombinant fragment of humanized anti-CD3 (FvFcR) or recombinant fragment chimeric anti-CD3 (FvFcM). After 72 hours, CD3+ T cells were isolated by negative selection using magnetic beads and total RNA was extracted with the RNeasy kit (Qiagen). Paired-end cDNA reads (150bp) were generated using the HiSeq 2500 Sequencing system (Illumina) located at the NGS Overseas Project Manager, Next Generation Sequencing Division, Macrogen, Inc. (Seoul, Korea). Quality check of the paired-end reads was performed using FASTQC. The reads were aligned to the human genome refence downloaded from the UCSC Genome Browser database using open source segemehl_0_2_0. The aligned files were ordered and indexed using Samtools followed by read count using HTSeq-count. Statistical analysis was done using the R environment for statistical computing. Gene model quantification were performed using the Bioconductor package DESeq2. Results: Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the human genome and identified 7089 transcripts in the T cell stimulated with OKT3, 2425 transcripts with FvFc R and 1406 with FvFc M. RNA-seq data confirmed stable expression of some known housekeeping genes, and 3 of these were validated with qRT-PCR. We found 860 genes there are equally regulated among the treatments, considering a padj ≤ 0.05. Altered expression of 35 genes was confirmed with qRT-PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Conclusions: In conclusion, we had used a deep transcriptome sequencing method for comparing three anti-CD3 antibodies in terms of gene ontology enrichment and immunological markers expression. The present data showed that both recombinant antibodies induced a compatible expression profile, suggesting they could be tested as substitute in human pre-clinical trials. Moreover, the proposed methodology is amenable to be more generally applied for molecular comparison purposes.
2019-08-07 | GSE112899 | GEO
Project description:This study uses whole-genome bisulfite sequencing to characterize the methylomes of the AOM/DSS mouse model at single-base resolution. In this model, mice are treated with dextran sodium sulfate (DSS) to induce colitis. When this treatment is preceded by injections of the weak carcinogen azoxymethane (AOM) the mice develop intestinal tumors. Our results identify hypermethylated DMVs as a prominent feature of the colitis methylome that is conserved in intestinal adenocarcinomas. Further analyses reveal a subset of DMV-associated genes, expressed in normal intestinal epithelial cells, that were silenced and hypermethylated in inflamed and cancerous intestinal cells. Together, these findings provide strong support for the hypothesis that inflammatory signals induce a higher risk for cancer development by manipulating the epigenome. . Whole genome methylation analysis of M. musculus. Three conditions were sequenced analyzed, the first is an untreated control, the second corresponds to inflammation, the third to cancer induced by inflammation. All three conditions were analyzed using three replicates.
2015-06-17 | E-GEOD-57527 | biostudies-arrayexpress