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Links from GEO DataSets

Items: 16

1.

Ets1 and IL17RA cooperate to regulate autoimmune responses as well as skin immunity to Staphylococcus aureus

(Submitter supplied) Autoimmune diseases display many changes to the immune environment. The lineage-specific transcription factor Ets1 has been associated with autoimmune diseases including SLE. Ets1KO mice develop significant autoimmune disease with an expansion of IL-17 expressing lymphocytes. To ascertain the role of IL-17 in the phenotype of Ets1KO mice, mice lacking both Ets1 and IL17Ra were generated. These double-knockout mice (DKO) were found to develop significant autoimmune disease characterized by development of spontaneous skin lesions. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: CSV, XLSX
Series
Accession:
GSE237696
ID:
200237696
2.

Ets1 suppresses the expression of key TFH genes to block TFH differentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL19057
16 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE110647
ID:
200110647
3.

Upregulation of TFH profile in absence of Ets1 expression

(Submitter supplied) To characterize the effect of loss of Ets1 in Non-TFH and TFH cells, we performed gene expression RNAseq analysis for T follicular helper (TFH) and Non-T follicular helper (Non-TFH) cells in WT (Ets1 fl/fl) and Ets1 KO (CD4-cre Ets1 fl/fl) mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: TXT
Series
Accession:
GSE110595
ID:
200110595
4.

Ets1 modulates epigentic landscape of key TFH genes in T naïve cells

(Submitter supplied) Ets1 can directly bind key TFH genes, regulating their expression . Loss of Ets1 results in the pre-mature expression of TFH-genes in Non-TFH cells. We wished to analyze if loss of Ets1 correlated with changes in chromatin accessibility especially in TFH gene loci.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: BIGWIG
Series
Accession:
GSE110594
ID:
200110594
5.

Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses

(Submitter supplied) To identify the molecular mechanisms responsible for enhanced atopic dermatitis (AD) pathogenesis upon Ets1 deficiency in CD4+ T cells, we compared transcriptome profile between CD4+ T cells from littermate control (LMC) and Ets1ΔdLck mice at the peak of AD progression by performing RNA-seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: TXT
Series
Accession:
GSE122795
ID:
200122795
6.

IκBζ-deficient epidermis mediates systemic autoimmune inflammation via skin dysbiosis.

(Submitter supplied) Skin microbiota affect systemic inflammation through mechanisms that have not been completely elucidated. We previously demonstrated that keratinocyte-specific IκBζ-deficient mice spontaneously develop autoimmune inflammation resembling human Sjögren syndrome. In this study, we examined how IκBζ-deficient epidermis dictates systemic autoimmune inflammation onset. To examine if IκBζ-deficient keratinocytes are susceptible to apoptotic stimuli in a steady state, we performed microarray analysis of untreated murine back epidermis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
2 Samples
Download data: TXT
Series
Accession:
GSE165515
ID:
200165515
7.

Th17 cell plasticity towards a T-bet-dependent Th1 phenotype is required for bacterial control in Staphylococcus aureus infection

(Submitter supplied) Th17 cells are involved in controlling systemic S. aureus infections especially in the kidney and T-bet expression during transdifferentiation by Th17 cells is required for bacterial clearance.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE199857
ID:
200199857
8.

Expression data of ILC2 cells from Ets1-deleted and littermate control mice

(Submitter supplied) The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
4 Samples
Download data: CEL
Series
Accession:
GSE79742
ID:
200079742
9.

Circadian Clock Protein CRY Regulates Autoimmunity

(Submitter supplied) The circadian system regulates numerous physiological processes including the adaptive immune system. Here we show that mice deficient for the circadian genes Cry1 and Cry2, (DKO) display an autoimmune phenotype including higher serum IgG concentration, presence of serum anti-nuclear antibodies, precipitation of IgG, IgM and complement 3 in glomeruli, and massive infiltrations of leukocytes into the lung and kidney. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE87467
ID:
200087467
10.

Bach2 deficiency leads to spontaneous expansion of IL-4-producing T follicular helper cells and autoimmunity

(Submitter supplied) The transcription factor Bach2 is a critical negative regulator of Tfh cell differentiation, especially IL-4 subset. Tfh cells from the mesenteric lymph nodes of WT and Bach2 CD4 conditional KO mice were collected to process the Rna-seq. Mechanistically, Bach2 may limit abnormal IL-4-produicng Tfh cell formation by repressing c-Maf, CXCR5 and IL-4.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
6 Samples
Download data: CSV
Series
Accession:
GSE135087
ID:
200135087
11.

RNA-seq analysis of IL-1B and IL-36 responses in epidermal keratinocytes identifies a shared MyD88-dependent gene signature

(Submitter supplied) IL-36 cytokines have recently emerged as mediators of inflammation in autoimmune conditions including psoriasis vulgaris (PsV) and generalized pustular psoriasis (GPP). This study used RNA-seq to profile the transcriptome of primary epidermal keratinocytes (KCs) treated with IL-1B, IL-36A, IL-36B or IL-36G. We identified some early IL-1B-specific responses (8 hours post-treatment), but nearly all late IL-1B responses were replicated by IL-36 cytokines (24 hours post-treatment). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
34 Samples
Download data: TXT
12.

The gene expression of MZ B cells and neutrophils after Staphylococcus aureus infection in B6 mice

(Submitter supplied) Marginal zone B cells can quickly respond to the bacterial invasion by providing the first-line of antibodies. Neutrophil can help marginal zone B cells activation and differentiation. We investigated the specific gene expression that interacts between the MZ B cells and neutrophils at the initial stage after Staphylococcus aureus infection.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL20258
4 Samples
Download data: CEL
Series
Accession:
GSE157176
ID:
200157176
13.

LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [BMDM]

(Submitter supplied) Patients with cutaneous T cell lymphoma (CTCL) experience high morbidity and mortality due to S. aureus skin infections and sepsis, but the causative immune defect is unclear. We propose that high levels of LAIR2 in CTCL suppress LAIR1 inhibitory signaling, promoting inflammation and tissue damage, which increases S. aureus susceptibility. Mice do not have a LAIR2 homolog, so we used Lair1 KO mice to model LAIR2 overexpression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TSV
Series
Accession:
GSE269178
ID:
200269178
14.

LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [abscess]

(Submitter supplied) Patients with cutaneous T cell lymphoma (CTCL) experience high morbidity and mortality due to S. aureus skin infections and sepsis, but the causative immune defect is unclear. We propose that high levels of LAIR2 in CTCL suppress LAIR1 inhibitory signaling, promoting inflammation and tissue damage, which increases S. aureus susceptibility. Mice do not have a LAIR2 homolog, so we used Lair1 KO mice to model LAIR2 overexpression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TSV
Series
Accession:
GSE269177
ID:
200269177
15.

IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247
29 Samples
Download data: MTX, TSV
Series
Accession:
GSE230513
ID:
200230513
16.

IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

(Submitter supplied) The complex system by which the skin regulates immune responses to the external environment is unclear. Here, we investigated cell-cell interactions underlying cutaneous defense against S. aureus. Single-cell transcriptomics (scRNA-Seq) and unbiased network analysis revealed unexpected, dominant IL-17-mediated dermal reticular fibroblast-to-neutrophil communication. Multi-faceted in vitro omics studies demonstrated that IL-17 synergized with several factors including TNF⍺ to induce fibroblast NFKBIZ and chemokine secretion. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247
23 Samples
Download data: CSV
Series
Accession:
GSE230511
ID:
200230511
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