To examine the differences between NOR1 and its fusion gene product EWS/NOR1, we compared the gene expression profiles of NOR1- and EWS/NOR1-overexpressing 293 cells.
Differential transactivation by orphan nuclear receptor NOR1 and its fusion gene product EWS/NOR1: possible involvement of poly(ADP-ribose) polymerase I, PARP-1.
No sample metadata fields
View SamplesGenome-wide expression analysis of two circadian oscillatory mechanisms in the mouse liver
Genome-wide expression analysis reveals 100 adrenal gland-dependent circadian genes in the mouse liver.
No sample metadata fields
View SamplesColon cancer invade to depper layer and the expression of major molecules at cancer front change. But the screening of expression changing at cancer front has not be adequtely clarified.
Microarray Analysis of Gene Expression at the Tumor Front of Colon Cancer.
No sample metadata fields
View SamplesTo clarify how Foxp3 regulates its target genes, we performed co-immunoprecipitation experiments and found that Foxp3 physically bound to AML1/Runx1 (Ono, M. et al, Nature, 2007). In this series of study, we compared gene regulations by AML1, wild type Foxp3, and a Foxp3 mutant with defective binding to AML1.
Foxp3 controls regulatory T-cell function by interacting with AML1/Runx1.
No sample metadata fields
View SamplesDendritic cells (DCs) are critical regulators of Foxp3+ regulatory T (Treg) cell-homeostasis. Recent reports have suggested that Langerin+ DCs, especially epidermal Langerhans cells (LCs), play an important role in inducing Treg cells. We investigated the roles of Langerin+ DCs in expanding Treg cells after ultraviolet B (UVB) exposure. We found that Treg cells were expanded in UVB-exposed skin in vivo even without Langerin+ DCs including LCs. In the UVB-exposed skin, Langerin- DCs showed a mature phenotype, and the Treg-expansion induced by UVB was significantly abrogated by CD86/CD80 blockade. Thus, maturing Langerin- DCs, rather than LCs and Langerin+ dermal DCs, are the main contributors to UVB-induced Treg expansion in the skin. These results indicate that a new mechanism for UVB-mediated tolerance, which can provide a new concept of treatment using DC-mediated tolerance.
Ultraviolet B-Induced Maturation of CD11b-Type Langerin<sup>-</sup> Dendritic Cells Controls the Expansion of Foxp3<sup>+</sup> Regulatory T Cells in the Skin.
Specimen part, Cell line
View SamplesGene expression profiles of Cbfb-deficient and control Treg cells were compared.
Indispensable role of the Runx1-Cbfbeta transcription complex for in vivo-suppressive function of FoxP3+ regulatory T cells.
Sex, Age, Specimen part
View SamplesDrosophila S2 cells treated with either GFP or spottes-dick dsRNA and incubated for 5 days. There are three replicates for each condition.
Spotted-dick, a zinc-finger protein of Drosophila required for expression of Orc4 and S phase.
No sample metadata fields
View SamplesWe describe GC-Tfr, a population of CD25 negative Foxp3 positive CXCR5hiPD1hiBCL6hi T-follicular regulatory cells that preferentially localise in the germinal centers. Male C57BL/6 Foxp3-DTR-GFP reporter mice were vaccinated with NP-Ova in Alum and 7 days later cells sorted before RNA-sequencing. Analysis revealed that GC-Tfr have a gene expression pattern equidistant between Tregs and Tfh, but fundamentally retain their suppressive characteristics as regulatory cells.
A distinct subpopulation of CD25<sup>-</sup> T-follicular regulatory cells localizes in the germinal centers.
Sex, Specimen part, Cell line
View SamplesT-follicular helper cells (Tfh) differentiate through a multistep process culminating in germinal center (GC) resident GC-Tfh that provide support to GC B-cells. T-follicular regulatory cells (Tfr) have been shown to have critical roles in the control of Tfh and germinal center formation. While Tfh cells are inhibited by IL-2, Treg cells depend on it. Here we describe a novel CD25 negative subset within both murine and human PD1+CXCR5+Foxp3+ Tfr that is preferentially located in the GC and can be clearly differentiated from non-GC Tfr, Tfh and effector Tregs by expression of a wide range of molecules. In comparison to Tfr and effector Tregs, GC-Tfr cells partially downregulate IL-2 dependent canonical Treg features, but retain suppressive function, while simultaneously upregulating genes associated with Tfh and GC-Tfh. We suggest that, similar to Tfh, Tfr follow a differentiation pathway culminating in a distinct GC resident subset, GC-Tfr.
A distinct subpopulation of CD25<sup>-</sup> T-follicular regulatory cells localizes in the germinal centers.
Sex, Age, Specimen part
View SamplesAnalysis of Foxp3(+)epigenetics(-) T cells, Foxp3(-)epigenetics(+) T cells, and Foxp3(+)epigenetics(+) T cells. Results indicate regulatory T cell (Treg) ontogenesis requires two independent processes, expression of the transcription factor Foxp3 and establishment of Treg epigenetic programs induced by T cell receptor (TCR) stimulation.
T cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development.
Specimen part
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