refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 49 results
Sort by

Filters

Technology

Platform

accession-icon SRP071123
Classical dendritic cells are required for dietary antigen-mediated peripheral regulatory T cell and tolerance induction I
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬– cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11b– cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Overall design: Four dendritic cell subpopulations from mouse mesenteric lymphnodes were sorted and compared in their gene expression profile

Publication Title

Classical dendritic cells are required for dietary antigen-mediated induction of peripheral T(reg) cells and tolerance.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP071124
Classical dendritic cells are required for dietary antigen-mediated peripheral regulatory T cell and tolerance induction II
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬– cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11b– cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Overall design: Sorted naïve CD45.1 OT-II CD4 T cells were co-cultured with four dendritic cell subpopulations sorted from mouse mesenteric lymphnodes. 24h later OT-II cells were sorted again and compared in their gene expression profile.

Publication Title

Classical dendritic cells are required for dietary antigen-mediated induction of peripheral T(reg) cells and tolerance.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP064961
Comparison between lamina propria macrophages and muscularis macrophages
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Lamina propria and muscularis macrophages, were sorted at steady steate and 2h after oral exposure to an attenuated form of Salmonella, comparison among these populations showed that the muscularis macrophages quckly respond to the presence of intestinal bacteria, upregulating some important tissue protective genes. Overall design: intestinal macrophages from 3 mice were pooled into one RNA sample, the experiment was done control X infected and was repeated twice

Publication Title

Neuro-immune Interactions Drive Tissue Programming in Intestinal Macrophages.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE60356
Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Retinoic acid is essential for Th1 cell lineage stability and prevents transition to a Th17 cell program.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE60354
Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [Affymetrix experiments]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version)

Description

CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies identify RA-RARa as a key component of the regulatory network governing Th1 cell fate and define a new paradigm for the development of pathogenic Th17 cells. These findings have important implications for autoimmune diseases in which dysregulated Th1-Th17 responses are observed.

Publication Title

Retinoic acid is essential for Th1 cell lineage stability and prevents transition to a Th17 cell program.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP185583
Vasculature-associated fat macrophages readily adapt to inflammatory and metabolic challenges
  • organism-icon Mus musculus
  • sample-icon 152 Downloadable Samples
  • Technology Badge IconNextSeq 500, Illumina HiSeq 2500

Description

We show that the epididymal white adipose tissue harbors 4 subpopulations of macrophages (VAM1, VAM2, PreVAM and DPs), 2 subpopulations of Dendritic Cells (CD11B+CD103- and CD11B-CD103+) and monocytes. VAMs display a gene signature enriched in pathways related to anti-inflammatory/ detoxifying and repair processes. Our gene expression work shows no evidence of an M2 to a Classically Activated/M1 shift during diet-induced obesity (DIO). Gene expression of VAMs or DP macrophages cannot be defined as M1 or M1-like. Our data are more compatible with the category of “Metabolically-activated” macrophages (MMe) Overall design: Examination of RNA expression changes in different epididymal adipose tissue myeloid subpopulations in lean versus obese animals harboring metabolic syndrome

Publication Title

Vasculature-associated fat macrophages readily adapt to inflammatory and metabolic challenges.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE41257
Transcriptional changes in intraepithelial CD4 lymphocytes
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We investigated transcriptional changes in CD4CD8aa and CD4 intraepthelial lymphocytes.

Publication Title

Transcriptional reprogramming of mature CD4⁺ helper T cells generates distinct MHC class II-restricted cytotoxic T lymphocytes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE90954
Effect of TGFb treatment (1 ng/ml) on gene expression in Hepa1-6 cells
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The goal of the study is a high-throughput evaluation of the effect of TGFb treatment on gene expression.

Publication Title

Resolving the Combinatorial Complexity of Smad Protein Complex Formation and Its Link to Gene Expression.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE59761
Transcriptional co-factor Transducin beta-like (TBL) 1 acts as a checkpoint in pancreatic cancer malignancy
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer fatalities in Western societies, characterized by high metastatic potential and resistance to chemotherapy. Critical molecular mechanisms of these phenotypical features still remain unknown, thus hampering the development of effective prognostic and therapeutic measures in PDAC. Here we show that transcriptional co-factor Transducin beta-like (TBL) 1 was over-expressed in both human and murine PDAC. Inactivation of TBL1 in human and mouse pancreatic cancer cells reduced cellular proliferation and enhanced chemosensitivity, correlating with diminished glucose uptake, glycolytic flux, and PI3kinase signaling. TBL1 deficiency both prevented and reversed pancreatic tumor growth in mice, triggering transcriptional PI3kinase inhibition also in vivo. As TBL1 mRNA levels were also found to correlate with overall and disease-free survival in a cohort of human PDAC patients and to predict therapy responsiveness in these subjects, TBL1 expression may serve both as a novel prognostic marker and molecular target in the treatment of human PDAC.

Publication Title

Transcriptional co-factor Transducin beta-like (TBL) 1 acts as a checkpoint in pancreatic cancer malignancy.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE17096
mRNA composition of IRP1 mRNPs in mouse tissues
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Affymetrix microarrays were used to determine the mRNA composition of mRNPs obtained by immunoprecipitation with IRP1 (iron regulatory protein 1).

Publication Title

Identification of target mRNAs of regulatory RNA-binding proteins using mRNP immunopurification and microarrays.

Sample Metadata Fields

Sex

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact