Similar Datasets
Project description:48hr 2a3 vs YTS177 CD4+ PLN T cell Microarray
| PRJNA744474 | ENA
Project description:How do Treg cells control an autoimmune lesion? We depleted Foxp3+ Treg cells in autoimmune prone TCR transgenic BDC2.5 mice on the NOD background Kinetic of gene-expression changes in CD4 T cells isolated for pancreas and pancreas draining lymph node (PLN) of Foxp3-DTR.BDC2.5/NOD mice after Treg cell ablation Keywords: T cell activation/ differentiation after Treg depletion timecourse CD4 T cells were isolated from pancreas and PLN at 0, 15 and 24 hours after diphtheria toxin application into 4-6 week old female Foxp3-DTR.BDC2.5/NOD transgenic mice
2009-10-15 | E-GEOD-18136 | biostudies-arrayexpress
Project description:These mice have been genetically modified so that the mouse PLN gene has been replace with the human PLN gene. Phopspholamban (PLN), the reversible inhibitor of the sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a), is a key regulator of myocyte Ca2+-cycling with a significant role in heart failure. We previously showed that the single amino acid difference between human and mouse PLN results in increased inhibition of Ca2+-cycling, cardiac remodeling and attenuated stress responses, in transgenic mice expressing the human PLN in the null background (hPLN). This set of microarray experiments aimed at deciphering the molecular mechanisms implicated in this process.
2011-12-15 | GSE20172 | GEO
Project description:How do Treg cells control an autoimmune lesion? We depleted Foxp3+ Treg cells in autoimmune prone TCR transgenic BDC2.5 mice on the NOD background Kinetic of gene-expression changes in CD4 T cells isolated for pancreas and pancreas draining lymph node (PLN) of Foxp3-DTR.BDC2.5/NOD mice after Treg cell ablation Keywords: T cell activation/ differentiation after Treg depletion timecourse
2009-10-15 | GSE18136 | GEO
Project description:These mice have been genetically modified so that the mouse PLN gene has been replace with the human PLN gene. Phopspholamban (PLN), the reversible inhibitor of the sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a), is a key regulator of myocyte Ca2+-cycling with a significant role in heart failure. We previously showed that the single amino acid difference between human and mouse PLN results in increased inhibition of Ca2+-cycling, cardiac remodeling and attenuated stress responses, in transgenic mice expressing the human PLN in the null background (hPLN). This set of microarray experiments aimed at deciphering the molecular mechanisms implicated in this process. 6 wild type, 6 transgenic mice. All at 11 weeks of age. FVB/N background. Whole hearts isolated, snap frozen and used for total RNA extraction.
2011-12-15 | E-GEOD-20172 | biostudies-arrayexpress
Project description:Mice were immunized with either MOG35-55 in CFA or with CFA alone and 14 days later PLN cells were isolated and stimulated in vitro with MOG35-55 for 3 days followed by CD4+ T cell sorting. Microarray analysis of miRNA expression profiles was performed comparing sorted CD4+ T cells from MOG35-55 in CFA immunized mice to CD4+ T cells from mice immunized with CFA alone. The data are from magnetic beads sorted CD4+ T cells from peripheral lymph nodes from 5 pooled animals per data point
2011-04-22 | E-GEOD-28473 | biostudies-arrayexpress
Project description:Aims: A mutation in the phospholamban (PLN) gene, leading to deletion of Arg14 (R14del), has been associated with malignant arrhythmias and ventricular dilation. Identifying pre-symptomatic carriers with vulnerable myocardium is crucial because arrhythmia can result in sudden cardiac death, especially in young adults with PLN-R14del mutation. This study aimed at assessing the efficiency and efficacy of in vivo genome editing, using CRISPR/Cas9 and a cardiotropic adeno-associated virus (AAV9), in improving cardiac function in young adult mice expressing the human PLN-R14del. Methods and Results: Humanized mice were generated expressing human wild-type (hPLN-WT) or mutant (hPLN-R14del) PLN in the heterozygous state, mimicking human carriers. Cardiac magnetic resonance imaging at 12 weeks of age showed bi-ventricular dilation and increased stroke volume in mutant vs. WT mice, with no deficit in ejection fraction or cardiac output. Challenge of ex vivo hearts with isoproterenol and rapid pacing unmasked higher propensity for sustained ventricular tachycardia (VT) in hPLN-R14del relative to hPLN-WT. Specifically, the VT threshold was significantly reduced (20.3±1.2 Hz in hPLN-R14del vs. 25.7±1.3 Hz in WT, p<0.01) reflecting higher arrhythmia burden. To inactivate the R14del allele, mice were tail-vein-injected with AAV9.CRISPR/Cas9/gRNA or AAV9 empty capsid (controls). CRISPR-Cas9 efficiency was evaluated by droplet digital PCR and NGS-based amplicon sequencing. In vivo gene editing significantly reduced end diastolic and stroke volumes in hPLN-R14del CRISPR-treated mice compared to controls. Susceptibility to VT was also reduced, as the VT threshold was significantly increased relative to controls (30.9±2.3 Hz vs. 21.3±1.5 Hz; p<0.01). Conclusions: This study is the first to show that disruption of hPLN-R14del allele by AAV9- CRISPR/Cas9 improves cardiac function and reduces VT susceptibility in humanized PLN-R14del mice, offering preclinical evidence for translatable approaches to therapeutically suppress the arrhythmogenic phenotype in human patients with PLN-R14del disease.
2023-03-11 | PXD031612 | Pride
Project description:We identified DCIR2+DCs but not DEC205+DCs as able to induce peripheral T cell tolerance in pre-diabetic autoimmune NOD mice. To determine what distinct genetic programs are elicited in the auto-reactive CD4 T cells early after stimulation by these two DC subsets, we utilized adoptive transfer of BDC2.5 CD4 T cells into NOD mice, which were then given chimeric antibody to deliver the beta-cell specific antigen to either DCIR2+DCs or DEC205+DCs, leading to BDC2.5 CD4 T cell specific stimulation in vivo. The analysis shows that the negative transcriptional factor Zbtb32 (ROG) is up-regulated more in BDC2.5 CD4 T cells after stimulated with a antigen via DCIR2+DCs presentation, compared with DEC205+DCs, suggesting the involvement of Zbtb32 in DCIR2+DCs-mediated auto-reactive T cell tolerance in disease ongoing NOD mice. The BDC2.5 CD4 T cells after 14 hour of injection with a 100 ng of anti-DCIR2-BDC, anti-DEC205-BDC antibody, or PBS as a control to NOD mice, were sorted by BD FACSAria and their expression profile was analyzed using Affymetrix chips.
2015-07-01 | GSE69554 | GEO
Project description:Mice were immunized with either MOG35-55 in CFA or with CFA alone and 14 days later PLN cells were isolated and stimulated in vitro with MOG35-55 for 3 days followed by CD4+ T cell sorting. Microarray analysis of miRNA expression profiles was performed comparing sorted CD4+ T cells from MOG35-55 in CFA immunized mice to CD4+ T cells from mice immunized with CFA alone.
2011-04-22 | GSE28473 | GEO
Project description:We identified DCIR2+DCs but not DEC205+DCs as able to induce peripheral T cell tolerance in pre-diabetic autoimmune NOD mice. To determine what distinct genetic programs are elicited in the auto-reactive CD4 T cells early after stimulation by these two DC subsets, we utilized adoptive transfer of BDC2.5 CD4 T cells into NOD mice, which were then given chimeric antibody to deliver the beta-cell specific antigen to either DCIR2+DCs or DEC205+DCs, leading to BDC2.5 CD4 T cell specific stimulation in vivo. The analysis shows that the negative transcriptional factor Zbtb32 (ROG) is up-regulated more in BDC2.5 CD4 T cells after stimulated with a antigen via DCIR2+DCs presentation, compared with DEC205+DCs, suggesting the involvement of Zbtb32 in DCIR2+DCs-mediated auto-reactive T cell tolerance in disease ongoing NOD mice. The BDC2.5 CD4 T cells after 14 hour of injection with a 100 ng of anti-DCIR2-BDC, anti-DEC205-BDC antibody, or PBS as a control to NOD mice, were sorted by BD FACSAria and their expression profile was analyzed using Affymetrix chips. NOD mice with transferred BDC2.5 T cell were injected with 100 ng of anti-DCIR2-BDC (NOD_DCIR2-BDC), anti-DEC205-BDC antibody (NOD_DEC-BDC), or PBS (NOD_PBS) as a control. After 14 hours, BDC2.5 CD4 T cells were sorted by BD FACSAria and their expression profile was analyzed using Affymetrix microarray chips. Each sample has a biological duplicate. Raw data were preprocessed with the RMA algorithm in Partek, and averaged expression values were used for analysis.
2015-07-01 | E-GEOD-69554 | biostudies-arrayexpress