Comparison of transcriptome between control, Tcf1 long isoform (p45)-deficient, complete Tcf1-deficient DN3 thymoctyes Overall design: lineage-negative, CD4-, CD8-, CD44 low and CD25 high (DN3) thymocytes were sorted from control mice or those are deficient for either Tcf1 long isoforms (p45) or all Tcf1 proteins. Lck-Cre was used to ablate all Tcf1 proteins
Cutting Edge: β-Catenin-Interacting Tcf1 Isoforms Are Essential for Thymocyte Survival but Dispensable for Thymic Maturation Transitions.
Specimen part, Subject
View SamplesComparison of the transcriptome between control Tfh and Tcf1 long isoform-deficient Tfh cells Overall design: SMARTA CD4+ T cells (control or Tcf1 long isoform deficient) were adoptively transferred into B6.SJL recipient mice and then infected with LCMV-Arm. On day 8 after infection, the splenocytes were isolated, and CD45.2+CD4+CXCR5+PD-1 negative cells were sorted as Tfh cells and used in RNAseq analysis.
Differential Requirements for Tcf1 Long Isoforms in CD8<sup>+</sup> and CD4<sup>+</sup> T Cell Responses to Acute Viral Infection.
Specimen part, Subject
View SamplesComparison of transcriptome between GFP-RV+ Th1 cells and Lef1-RV+ Th1 cells Overall design: B6 mice received GFP-RV+ or Lef1-RV+ LCMV gp specific TCRtg Smarta cells and were infected with LCMV. On four days after infection, splenocytes were collected to sort CXCR5- Th1 cells per genotype. Contributor: LIAI RNAi Center (LIAI)
LEF-1 and TCF-1 orchestrate T(FH) differentiation by regulating differentiation circuits upstream of the transcriptional repressor Bcl6.
No sample metadata fields
View SamplesComparison of transcriptome between control and Tcf1/Lef1-deficient germinal center Tfh (GC-Tfh) cells Overall design: Control mice or those are deficient for Tcf1 and Lef1 transcription factors were infected with vaccinia virus. On day 8 after infection, the splenocytes were isolated and surface stained to identify CD44-high, CD62L-low, GFP+, CD4+ T cells. From these cells, PD-1+, CXCR5+ GC-Tfh cells were sorted for RNAseq analysis
LEF-1 and TCF-1 orchestrate T(FH) differentiation by regulating differentiation circuits upstream of the transcriptional repressor Bcl6.
No sample metadata fields
View SamplesOur experiments aimed to investigate the landscape of enhancers and super-enhancers in naïve, effector and memory CD8+ T cells. Here we mapped four histone modification marks and gene expression in naive, effector, and memory cells after viral infection. Our results suggest that the chromatin environment at regulatory DNA sequences in TCM is more permissive than in TN and TE. We further predicted the enhancers and their targets, and constructed transcriptional regulatory networks (TRNs) in three T cell stages. We have identified a highly dynamic repertoire of the enhancers and their targets during CD8 T cell responses, as 77% of the enhancers and 82% of the enhancer-promoter interactions are stage-specific. Our results suggest the dynamic change of enhancer activity during cell stage transition leads to TRN rewiring, which explains the expression change of the key factors of T cell function. Overall design: We performed ChIP-Seq for 4 histone modification markers and RNA-Seq experiments in three CD8+ T cell differentiation stages.
CD8<sup>+</sup> T Cells Utilize Highly Dynamic Enhancer Repertoires and Regulatory Circuitry in Response to Infections.
Cell line, Subject
View SamplesOur experiments aimed to investigate the landscape of enhancers and super-enhancers in naïve, effector and memory CD8+ T cells. Here we mapped four histone modification marks and gene expression in naive, effector, and memory cells after viral infection. Our results suggest that the chromatin environment at regulatory DNA sequences in TCM is more permissive than in TN and TE. We further predicted the enhancers and their targets, and constructed transcriptional regulatory networks (TRNs) in three T cell stages. We have identified a highly dynamic repertoire of the enhancers and their targets during CD8 T cell responses, as 77% of the enhancers and 82% of the enhancer-promoter interactions are stage-specific. Our results suggest the dynamic change of enhancer activity during cell stage transition leads to TRN rewiring, which explains the expression change of the key factors of T cell function. Overall design: We performed RNA-Seq experiments in WT and Tcf1/Lef1 difficient CD8 cells, and performed Hi-C experiments in WT cells.
CD8<sup>+</sup> T Cells Utilize Highly Dynamic Enhancer Repertoires and Regulatory Circuitry in Response to Infections.
Cell line, Subject
View SamplesHuman CD4+ T cells and CD14+ monocytes from healthy donors were co-cultured with anti-CD3 for three days in the presence or absence of TNF-alpha mAb (Adalimumab). Classical Th17 cells (Th17) or those generated in the presence of the inhibitor (iTh17) were then sorted and analyzed by full transcriptome microarray analysis.
TNF-α blockade induces IL-10 expression in human CD4+ T cells.
Specimen part, Treatment, Subject
View SamplesWe run microarrays from three per group Sv129 female mice, ten weeks old, which were maintained at 28C (warm conditions) or 6 C (cold stimulated) for ten days, while standard animal house temperature is 22 C.
Brown and white adipose tissues: intrinsic differences in gene expression and response to cold exposure in mice.
Sex, Age, Specimen part
View SamplesWe used high throughput sequencing to analyze the transcriptional profiling of EVT. By comparing the transcriptional profiling of EVT with or without H19 knockdown, numerous genes showed significantly altered expression as a result of H19 repression. Overall design: HTR cells were transfected with either control siRNA or siH19. 48h later after transfection, total RNA was extracted for library preparation and RNA-seq analysis to compare trancript profiles between siCon and siH19 cells.
H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.
Cell line, Subject, Time
View SamplesPatients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.
Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
Sex, Age, Specimen part, Disease
View Samples