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accession-icon GSE56017
Mertk negatively regulates adaptive immunity
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Tolerogenic dendritic cells (tol-DCs) offer a promising therapeutic potential for autoimmune diseases. Tol-DCs have been reported to inhibit immunogenic responses, yet little is known about the mechanisms controlling their tolerogenic status, as well as associated specific markers. Here we show that the anti-inflammatory TAM receptor tyrosine kinase MERTK, is highly expressed on clinical grade dexamethasone-induced human tol-DCs and mediates their tolerogenic effect. Neutralization of MERTK in allogenic mixed lymphocyte reactions as well as autologous DC-T cell cultures leads to increased T cell proliferation and IFN-g production. Additionally, we identify a previously unrecognized non-cell autonomous regulatory function of MERTK expressed on DCs. Recombinant Mer-Fc protein, used to mimic MERTK on DCs, suppresses nave and antigen-specific memory T cell activation. This mechanism is mediated by the neutralization of the MERTK agonist Protein S (PROS1) expressed by T cells. We find that MERTK and PROS1 are expressed in human T cells upon TCR activation and drive an autocrine pro-proliferative mechanism. Collectively, these results suggest that MERTK on tol-DCs directly inhibits T cell activation through the competition for PROS1 interaction with MERTK in the T cells. Targeting MERTK may provide an interesting approach to effectively increase or suppress tolerance for the purpose of immunotherapy.

Publication Title

MERTK as negative regulator of human T cell activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15316
Differential expression of rituximab responders vs. non responders on 3 different blood cell types
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconSentrix Human-6 Expression BeadChip

Description

New and effective therapeutical options are available for the treatment of Rheumatoid Arthritis. One of such treatments is rituximab, and chimeric anti-CD20 antibody that selectively depletes the CD20+ B cell subpopulation.

Publication Title

Identification of candidate genes for rituximab response in rheumatoid arthritis patients by microarray expression profiling in blood cells.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE12051
Microarray predictor of response to infliximab in rheumatoid arthritis (RA) patients
  • organism-icon Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconSentrix Human-6 Expression BeadChip

Description

We sought to find a gene-expression multigene predictor of response to infliximab therapy in Rheumatoid Arthritis patients. Using internal and external cross-validation systems we have built and validated an 8-gene predictor for response to infliximab.

Publication Title

An eight-gene blood expression profile predicts the response to infliximab in rheumatoid arthritis.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

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accession-icon GSE18801
Transcriptional profile of isoproterenol-induced cardiomyopathy and comparison to exercise-induced cardiac hypertrophy
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We performed microarray analyses on RNA from mice with isoproterenol-induced cardiac hypertrophy and mice with exercise-induced physiological hypertrophy and identified 865 and 2,534 genes that were significantly altered in pathological and physiological cardiac hypertrophy models, respectively.

Publication Title

Transcriptional profile of isoproterenol-induced cardiomyopathy and comparison to exercise-induced cardiac hypertrophy and human cardiac failure.

Sample Metadata Fields

Specimen part

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accession-icon SRP113285
RNA-sequencing of Mbd3-null and control haematopoietic stem cell and lymphoid progenitor cell populations
  • organism-icon Mus musculus
  • sample-icon 78 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To determine the role of Mbd3/NuRD in lymphopoiesis, gene expression in purified populations of Mbd3-deleted and control lymphoid progenitor cells was analysed using RNA-seq. Overall design: Mbd3-deficient and control lymphoid progenitors were isolated from mouse bone marrow by flow cytometry, including haematopoietic stem cells (HSCs), lymphoid-primed multipotent progenitors (LMPPs), all-lymphoid progenitors (ALPs) and B cell-biased lymphoid progenitors (BLPs). RNA-seq was performed on 100 HSCs or 150 cells from the other populuations, using the previously described smartseq2 protocol for RNA-seq of small numbers of cells (Picelli et al. (2014) Nature protocols 9:171).

Publication Title

Mbd3/NuRD controls lymphoid cell fate and inhibits tumorigenesis by repressing a B cell transcriptional program.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon SRP098738
An autofluorescence-based method for the isolation of highly purified ventricular cardiomyocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Profiling of the transcriptome of FITChigh/FSCdim and FITCdim/FSChigh sub-populations. Three biological replicates were profiled for each cell type. Overall design: Profiling of the transcriptome of FITChigh/FSCdim and FITCdim/FSChigh sub-populations. Three biological replicates were profiled for each cell type.

Publication Title

An autofluorescence-based method for the isolation of highly purified ventricular cardiomyocytes.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE17844
Basal expression in daDREAM transgenic mouse hippocampus
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Changes in nuclear Ca2+ homeostasis activate specific gene expression programs and are central to the acquisition and the plastic storage of memories. DREAM /KChIP proteins form heterotetramers that bind DNA and repress transcription in a Ca2+-dependent manner. Single ablation of one member of the DREAM/KChIP family may result in a mild or the absence of phenotype due to partial gene compensation. To study the function of DREAM/KChIP proteins in the brain, we used transgenic mice expressing a Ca2+-insensitive/CREB-independent dominant active mutant DREAM (daDREAM). We show that daDREAM controls the expression of several activity-dependent transcription factors including Npas4, Nr4a1, Mef2C, JunB and c-Fos, as well as the chromatin modifying enzyme Mbd4 and proteins related to actin polymerization like Arc and gelsolin. Thus, directly or through these targets, expression of daDREAM in the forebrain resulted in a complex phenotype characterized by i) impaired learning and memory, ii) loss of recurrent inhibition and enhanced LTP in the dentate gyrus without affecting Kv4-mediated potassium currents, and iii) modified spine density in DG granule neurons. Our results propose DREAM as a master-switch transcription factor regulating several activity-dependent gene expression programs to control synaptic plasticity, learning and memory.

Publication Title

DREAM controls the on/off switch of specific activity-dependent transcription pathways.

Sample Metadata Fields

Specimen part

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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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