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Links from GEO DataSets

Items: 12

1.

Androgens Alleviate Allergic Airway Inflammation by Suppressing Cytokine Production of Th2 Cells

(Submitter supplied) This study reveraled that androgen signaling suppresses differentiation and cytokine production of Th2 cells by inducing DUSP-2, explaining, in part, the sex bias of asthma after adolescence.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
8 Samples
Download data: CSV
Series
Accession:
GSE200840
ID:
200200840
2.

Notch signaling licenses allergic airway inflammation by promoting lymph node egress of Th2 cells

(Submitter supplied) Transcriptome analyses of wildtype and Notch-deficient Th2 cells from mouse models of allergic airway inflammation.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
17 Samples
Download data: TXT
Series
Accession:
GSE125358
ID:
200125358
3.

Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL4134 GPL10333
6 Samples
Download data: GPR, TXT
Series
Accession:
GSE39863
ID:
200039863
4.

Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses [A]

(Submitter supplied) T helper type 2 (Th2) responses are crucial for defense against infections by helminths and are responsible for the development of allergic reactions that can lead to severe clinical disorders, such as asthma or anaphylaxis, and ultimately to death. The induction of Th2 responses requires a specific activation process, triggered by specialized dendritic cells (DCs), by which naive CD4+ Th0 cells acquire the capacity to produce Th2 cytokines. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL4134
4 Samples
Download data: GPR
Series
Accession:
GSE39862
ID:
200039862
5.

Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses [B]

(Submitter supplied) T helper type 2 (Th2) responses are crucial for defense against infections by helminths and are responsible for the development of allergic reactions that can lead to severe clinical disorders, such as asthma or anaphylaxis, and ultimately to death. The induction of Th2 responses requires a specific activation process, triggered by specialized dendritic cells (DCs), by which naive CD4+ Th0 cells acquire the capacity to produce Th2 cytokines. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10333
2 Samples
Download data: TXT
Series
Accession:
GSE39858
ID:
200039858
6.

To Study the effects of antioxidant on allergic airways inflammations

(Submitter supplied) Ragweed challenge in Ragweed (RWE) sensitized animals generates Reactive oxygen species (ROS) in the airway epithelium and induces allergic airway inflammation. We want to study the genes induced by ROS generated by RWE. This goal can be achieved by comparing PBS challenge vs. RWE challenge. Keywords: Infection
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
7 Samples
Download data: CEL, CHP
Series
Accession:
GSE18083
ID:
200018083
7.

Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

(Submitter supplied) Bcl6 play a key role in CD4+ T cell development including follicular regulatory T cells. However, the role of Bcl6 in Treg cells in context of allergic inflammation was not fully understood. In this study, we describe the role of Bcl6 in development and function of ST2+Treg cells by analyzing ST2+Treg cell RNA seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: XLSX
Series
Accession:
GSE136556
ID:
200136556
8.

Real-time quantitative PCR analysis of mRNA from lungs of WT and Pglyrp1-/- mice sensitized with HDM

(Submitter supplied) Wild type (WT) and Pglyrp1-/- mice were treated with PBS or sensitized 5 days/week for 3 or 5 weeks with 10 µl per application of 2.5 mg/ml of purified house dust mite allergen. 3 days after the last sensitization the lungs were removed and homogenized, and RNA was isolated from the right lobes using the TRIZOL method. Quantitative reverse transcription real-time PCR (qRT-PCR) was used to quantify the amounts of mRNA in the lungs using custom RT2 Profiler PCR Arrays designed by us and manufactured by Qiagen/SA Biosciences.
Organism:
Mus musculus
Type:
Expression profiling by RT-PCR
Platform:
GPL16426
18 Samples
Download data: TXT
Series
Accession:
GSE43137
ID:
200043137
9.

Androgen regulation of T cell-intrinsic mechanisms contributes to the sex bias in autoimmunity.

(Submitter supplied) Major autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis, rheumatoid arthritis and Graves’ disease display a striking female bias, with a female-to-male incidence ratio ranging up to 9:1 in SLE. Sex hormones contribute to protection of males from autoimmunity, but precise molecular mechanisms of such protection are poorly understood. Here, we find that Androgen Receptor (AR), a nuclear receptor regulating a plethora of genes, is active in T cells during development and regulates directly genes involved in T cell activation or indirectly through regulation of other transcription factors. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL34328
6 Samples
Download data: MTX, TSV
Series
Accession:
GSE271153
ID:
200271153
10.

Sex bias in autoimmunity is driven by androgen regulation of T cell-intrinsic mechanisms

(Submitter supplied) Major autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis, rheumatoid arthritis and Graves’ disease display a striking female bias, with a female-to-male incidence ratio ranging up to 9:1 in SLE. Sex hormones contribute to protection of males from autoimmunity, but precise molecular mechanisms of such protection are poorly understood. Here, we find that Androgen Receptor (AR), a nuclear receptor regulating a plethora of genes, is active in T cells during development and regulates directly genes involved in T cell activation or indirectly through regulation of other transcription factors. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
3 Samples
Download data: TXT
Series
Accession:
GSE234134
ID:
200234134
11.

Effect of androgen receptor signaling on H3K27 trimethylation in Th17 cells

(Submitter supplied) Females have increased prevalence of many Th17-mediated diseases, including asthma. Androgen signaling decreases Th17-mediated airway inflammation, and Th17 cells rely on glutaminolysis. However, it remains unclear whether androgen receptor (AR) signaling modifies glutamine metabolism to suppress Th17-mediated inflammation. In this experiment, we conducted a CUT & RUN to determine how AR signaling modified histone 3 lysine 27 trimethylation in Th17 cells from WT males, WT females, and ArTfm male mice (n=3 from each group).
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: BW
Series
Accession:
GSE241823
ID:
200241823
12.

Effect of androgen on aldosterone and high salt induced aortic aneurysms in mice

(Submitter supplied) Aortic aneurysm is a highly age- and sex-dependent cardiovascular disease in human, which men are at 4 to 6 times higher risk than women. We recently established an age-dependent animal model in which aldosterone and high salt administration induces aortic aneurysms in 10-month-old wildtype male mice. But whether it exhibits sex differences as in human remains unknown. The current study reports that androgen is a main driver for the sexual dimorphic response to aldosterone and high salt induced aortic aneurysms in mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
15 Samples
Download data: TXT
Series
Accession:
GSE255682
ID:
200255682
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