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accession-icon GSE6813
Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The NOD (nonobese diabetic) mouse strain develops a characteristic autoimmune syndrome that closely resembles human type I diabetes. It has been suggested that NOD mice exhibit both numerical deficiency in CD4+CD25+ regulatory T cells (Treg) and reduced suppressive activity. We compared sorted CD4+CD25+ Tregs from the spleens of 6-7 week-old female NOD and nondiabetic B6.H2g7 mice. Tregs were 932% and 951% Foxp3+ in NOD and B6.H2g7 cells, respectively, on post-sort reanalysis. "Conventional" CD4+CD25- T cells (Tconv) are included as reference populations. Surprisingly, Treg "signature" is similar between the two strains, with only a few probesets that subtly deviate.

Publication Title

The defect in T-cell regulation in NOD mice is an effect on the T-cell effectors.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP018853
Altered microRNA expression in individuals at high risk of type 1 diabetes
  • organism-icon Homo sapiens
  • sample-icon 80 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina Genome Analyzer IIx

Description

Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic insulin-producing ß cells. CD4+ T cells are integral to the pathogenesis of T1D, but biomarkers that define their pathogenic status in T1D are lacking. miRNAs have essential functions in a wide range of tissues/organs, including the immune system. We reasoned that CD4+ T cells from individuals at high risk for T1D (pre-T1D) might be distinguished by an miRNA signature. We sorted CD4+ T cells from 9 healthy and 7 pre-T1D individuals into 6 subsets, namely naïve, resting regulatory (rTreg), activated regulatory (aTreg), transitional memory (Ttm), central memory (Tcm) and effector memory (Tem) cells, and then compared miRNA profiles between these subsets and between pre-T1D and healthy individuals by deep sequencing. Differential expression of miRNAs was detected in each of the CD4+ T cell subsets. For example, expression of miRNAs that induce apoptosis (miR-15a) or FOXP3 instability (miR-31) was increased in rTreg and aTreg cells, respectively, in pre-T1D individuals, whereas miR-150 was increased in Tem cells of pre-T1D individuals. Importantly, increased miR-150 expression could be detected by qRT-PCR in total CD4+ T and PBMCs of pre-T1D individuals. Consistent with it being a marker of pathogenic CD4+ T cells, we showed that miR-150 regulates IFN-? production in mouse CD4+ T cells. Thus, comprehensive profiling identifies miRNA profiles that not only distinguish CD4+ T cell subsets but also discriminate individuals with preclinical T1D. The ability to detect differentially expressed miRNAs in total CD4+ T cells or PBMCs should facilitate clinical application of miRNAs as biomarkers. Overall design: CD4+T cells from healthy and individuals at high risk for autoimmune type 1 diabetes were sorted into 6 subsets, which resulted in 80 samples, 38 for healthy and 42 for high risk individuals. Each sample was barcoded and miRNA libraries were constructed and subsequently subjected to deep-sequencing on the Illumina GAII or HiSeq platform. The Fastq files are have deconvoluted and stripped of the barcode adaptor sequences.

Publication Title

MicroRNAs in CD4(+) T cell subsets are markers of disease risk and T cell dysfunction in individuals at risk for type 1 diabetes.

Sample Metadata Fields

Subject

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accession-icon GSE52658
Dynamic developmental signaling logic underlying lineage bifurcations during human endoderm induction and patterning from pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Efficient endoderm induction from human pluripotent stem cells by logically directing signals controlling lineage bifurcations.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE52158
Dynamic developmental signaling logic underlying lineage bifurcations during human endoderm induction and patterning from pluripotent stem cells [Expression data set]
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The definitive endoderm germ layer is the provenance of multiple internal organs, including the lungs, liver, pancreas and intestines. Molecular events driving initial endoderm germ layer specification and subsequent anterior-posterior patterning of endoderm into distinct organ primordia remain largely cryptic.

Publication Title

Efficient endoderm induction from human pluripotent stem cells by logically directing signals controlling lineage bifurcations.

Sample Metadata Fields

Specimen part, Cell line

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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