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accession-icon GSE26568
Impact of KLF2 expression on T cell genetic program
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

On triggering of the T cell receptor CD8 T lymphocytes downregulate expression of the transcription factor KLF2. KLF2 expression remains low as these cells differentiate to Cytotoxic T lymphocytes (CTL) but may be re-expressed depending on the local environmental signals.

Publication Title

The impact of KLF2 modulation on the transcriptional program and function of CD8 T cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE27092
Expression data from P14 TCR cytotoxic T cells overexpressing HDAC7 phosphorylation deficient mutant
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The present study reports an unbiased analysis of the cytotoxic T cell serine-threonine phosphoproteome using high resolution mass spectrometry. Approximately 2,000 phosphorylations were identified in CTLs of which approximately 450 were controlled by TCR signaling. A significantly overrepresented group of molecules identified in the phosphoproteomic screen were transcription activators, co-repressors and chromatin regulators. A focus on the chromatin regulators revealed that CTLs have high expression of the histone deacetylase HDAC7 but continually phosphorylate and export this transcriptional repressor from the nucleus. HDAC7 dephosphorylation results in its nuclear accumulation and suppressed expression of genes encoding key cytokines, cytokine receptors and adhesion molecules that determine CTL function. The screening of the CTL phosphoproteome thus reveals intrinsic pathways of serine-threonine phosphorylation that target chromatin regulators in CTLs and determine the CTL functional program. We used Affymetrix microarray analysis to explore the molecular basis for the role of HDAC7 in CTLs and the impact of GFP-HDAC7 phosphorylation deficient mutant expression on the CTL transcriptional profile.

Publication Title

Phosphoproteomic analysis reveals an intrinsic pathway for the regulation of histone deacetylase 7 that controls the function of cytotoxic T lymphocytes.

Sample Metadata Fields

Specimen part

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accession-icon GSE33942
Role of PKD2 in TCR-induced transcriptional reprogramming of nave T cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Comparison of transcriptional profile of TCR stimulated P14-TCR wild-type and P14-PKD2 null murine lymph node cells

Publication Title

Protein kinase D2 has a restricted but critical role in T-cell antigen receptor signalling in mature T-cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE26290
Expression data from control and Phospholipid dependent kinase 1 (PDK1) null cytotoxic T-lymphocytes (CTL) and from control and Akt inhibitor treated CTL
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In cytotoxic T cells (CTL), Protein Kinase B /Akt is activated by the T cell antigen receptor (TCR) and the cytokine Interleukin 2 (IL2), in part by phosophorylation of Akt by Phospholipid dependent kinase 1 (PDK1).

Publication Title

Protein kinase B controls transcriptional programs that direct cytotoxic T cell fate but is dispensable for T cell metabolism.

Sample Metadata Fields

Specimen part

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accession-icon GSE70925
Effect of rapamycin and KU-0063794 on CTL gene expression
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Comparison of transcriptional profile of CD8 cytotoxic T lymphocytes terated with the mTORC1 inhibitor rapamycin or the mTOR inhibitor KU-0063794 and comparison with proteomic analysis.

Publication Title

The cytotoxic T cell proteome and its shaping by the kinase mTOR.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE46923
Systemic lupus erythematosus
  • organism-icon Homo sapiens
  • sample-icon 139 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment, Subject, Time

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accession-icon GSE46917
Differentially expressed transcripts in SLE blood monocytes according to their capacity to induce mixed lymphocytic reaction
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)

Description

We screened SLE monocytes from 19 SLE patients and selected 4 that induced CD4+ T cell proliferation in vitro and 4 that did not. CFSE labeled CD4-T cells (105) were incubated with SLE monocytes (2 x 104). Cells were harvested at 6 hours for RNA extraction.

Publication Title

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment, Subject, Time

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accession-icon GSE46911
Transcripts induced by recombinant IFNa in healthy blood monocytes at different time points
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a), Affymetrix Human Genome U133B Array (hgu133b)

Description

To explore the full extent of IFN-regulated transcriptional changes, we exposed monocytes from two healthy donors to recombinant type I IFN (IFN-2b) in vitro. RNA was extracted at different incubation times (1, 6, 24, 48 and 72 hrs) and the expression data was normalized to that of monocytes cultured with medium.

Publication Title

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment, Time

View Samples
accession-icon GSE46913
Transcripts differentially expressed in healthy blood mDCs compared to healthy monocytes
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)

Description

To directly compare the SLE monocyte transcriptional program with that of blood mDC precursors, we purified lineage HLA-DRhighCD11chigh mDCs and CD14+ monocytes from the blood of five healthy donors. Their gene expression profiles were then compared to those of blood SLE monocytes. An unsupervised clustering analysis of transcripts present in >20% of the samples classified healthy monocytes, SLE monocytes and healthy mDCs into three well defined groups. A supervised analysis was then performed to find genes: 1) differentially expressed in healthy mDCs compared to monocytes; 2) shared by healthy blood mDCs and SLE blood monocytes.

Publication Title

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE46907
Differentially expressed transcripts in SLE blood monocytes
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)

Description

To better characterize the molecules that could potentially confer antigen presenting capacity to SLE monocytes, we assessed their gene expression profile.

Publication Title

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

View Samples
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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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