Affymetrix Human Genome U133A platform was used to obtain gene expression profiles of 28 pathologically and clinically well characterized adenocarcinomas of the lung. In addition, EGFR status was determined by fluorescent in situ hybridization and immunohistochemistry.
Gene expression profiles of lung adenocarcinoma linked to histopathological grading and survival but not to EGF-R status: a microarray study.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Thymic negative selection is functional in NOD mice.
Sex, Age
View SamplesThe aim of this study was to quantify the impact of NOD genetic vatiation on thymic negative selection transcriptional programs.
Thymic negative selection is functional in NOD mice.
Sex, Age
View SamplesThe aim of this study was to quantify the impact of NOD genetic vatiation on the transcriptional programs induced by the alpha beta-TCR at the DN to DP transition in the BDC2.5 TCR Tg model
Thymic negative selection is functional in NOD mice.
Sex, Age
View SamplesWe obtained gene expression data and HD-SNP6.0 copy number data from PTL, PCNSL and PMLBCL samples and performed an integrative analysis on them. RNA was whole genome amplified using Nugen.
Targetable genetic features of primary testicular and primary central nervous system lymphomas.
Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PPAR-γ is a major driver of the accumulation and phenotype of adipose tissue Treg cells.
Sex, Age, Specimen part, Treatment
View SamplesWe identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To establish the role of Pparg in shaping the VAT Tregs gene profile and cell dynamics, Tregs from lymph nodes and visceral adipose tissue of mice sufficient and deficient of Pparg expression in Tregs were double sorted for microarray analysis.
PPAR-γ is a major driver of the accumulation and phenotype of adipose tissue Treg cells.
Sex, Age, Specimen part
View SamplesWe identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To explore the contribution of Pparg1 and 2 in the generation of the VAT Tregs-specific gene signatures, CD4+FoxP3- T cells were transduced with Foxp3+/- Pparg1 (or Pparg2), treated with Pioglitazone or vehicle, and double sorted for microarray analysis.
PPAR-γ is a major driver of the accumulation and phenotype of adipose tissue Treg cells.
Sex, Age, Specimen part, Treatment
View SamplesThe 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.
The defect in T-cell regulation in NOD mice is an effect on the T-cell effectors.
Age, Specimen part
View SamplesThe transcription factor Foxp3 is usually considered the master regulator for the CD4+CD25+ "Treg" lineage, which plays a key role in controlling immune and autoimmune responses, and is characterized by a unique transcriptional signature. We have performed a meta-analysis of this signature in Treg cells in several conditions to delineate the elements that can be ascribed to T cell activation, TGFbeta signaling, or Foxp3 itself. We find that these influences synergize to activate many of the signatures components. Foxp3 and TGFbeta signaling have interconnected relationships, as Foxp3 is induced by TGFbeta while enhancing TGFbetas positive feedback loop. Much of the Treg signature cannot be ascribed to Foxp3, as it contains gene clusters that are co-regulated, but cannot be transactivated, by Foxp3. This suggests that the Treg lineage is specified at a higher level of regulation, upstream of Foxp3, which does control some of the lineages essential immunoregulatory attributes.
Foxp3 transcription-factor-dependent and -independent regulation of the regulatory T cell transcriptional signature.
Age, Specimen part
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