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Links from GEO DataSets

Items: 12

1.

BET bromodomain inhibitor iBET151 impedes human ILC2 activation and prevents experimental allergic lung inflammation

(Submitter supplied) Group 2 innate lymphoid cells (ILC2) increase in frequency in eczema and allergic asthma patients, and thus represent a new therapeutic target cell for type-2 immune-mediated disease. The bromodomain and extra-terminal (BET) protein family of epigenetic regulators are known to support the expression of cell cycle and pro-inflammatory genes during type-1 inflammation, but have not been evaluated in type-2 immune responses. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
14 Samples
Download data: TXT
2.

RNA-seq of control and IL-33-treated WT and STAT KO ILC2s in vitro

(Submitter supplied) Group 2 innate lymphoid cell (ILC2), an innate counterpart of T helper 2 cell, plays a critical role in type 2 immune responses. However, the molecular regulation mechanism of ILC2 is still unclear. Here, we find that STAT3 signaling is essential for ILC2 effector function and could drive both acute and chronic allergic inflammation in the lung. Mechanistically, allergic alarmin IL-33 induces a non-canonical STAT3 phosphorylation at serine 727 in ILC2, which leads to its mitochondrial translocation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
8 Samples
Download data: TXT
Series
Accession:
GSE166081
ID:
200166081
3.

RNA-Seq of ILC2p WT

(Submitter supplied) We have generated RNA-seq of ILC2 progenitors form WT bone marrow mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
2 Samples
Download data: TXT
Series
Accession:
GSE97354
ID:
200097354
4.

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of CD200R engagment on sorted mouse pulmonary ILC2 Transcriptomes.

(Submitter supplied) The prevalence of asthma and airway hyperreactivity (AHR) is increasing at an alarming rate. Group 2 innate lymphoid cells (ILC2s) are copious producers of type 2 cytokines, which leads to AHR and lung inflammation. In this study, we demonstrate murine ILC2s express CD200 receptor (CD200R), and this expression is inducible. We ascertain CD200R engagement inhibits activation, proliferation, and type 2 cytokine production, revealing a potent immunoregulatory role for CD200–CD200R axis on ILC2s. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: XLS
Series
Accession:
GSE166889
ID:
200166889
5.

RNA-Seq analysis of mouse group 2 innate lymphoid cells (ILC2s) cultured with IL-33, IFN-g, and IL-27

(Submitter supplied) Purpose: We found that IFN-g and IL-27 had suppressive effects on ILC2s cultured with IL-33. The goal of this study is to clarify the expressions of RNA induced by IFN-g and IL-27 in ILC2s. Methods: ILC2s were isolated from fat-asociated lymphid clusters (FALC) of wild-type mice. They were cultured with IL-33 (10ng/ml), IL-33 + IFN-g (10ng/ml), or IL-33 + IL-27 (10ng/ml) for 48hrs. RNA was isolated by Allprep DNA/RNA Micro Kit (QIAGEN), and cDNA libraries were prepared by TruSeq RNA Sample Preparation kits v2 (Illumina) according to the manufacturer’s low sample protocol. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18480
9 Samples
Download data: TXT
Series
Accession:
GSE73272
ID:
200073272
6.

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

(Submitter supplied) Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
16 Samples
Download data: CEL
Series
Accession:
GSE81700
ID:
200081700
7.

Neuromedin U receptor-1 amplifies inflammatory lung innate lymphoid cells

(Submitter supplied) Type 2 innate lymphoid cells (ILC2s) promote mucosal homeostasis, yet also contribute to pathologic type 2 inflammation in allergic asthma. Alarmin cytokines produced by damaged and stressed epithelial cells, such as IL-25, activate ILC2s, but it remains unclear if these cytokines are unique in switching homeostatic ILC2s into pro-inflammatory cells that drive tissue inflammation. To identify molecular cues that modulate ILC responses to alarmins, we collected single-cell RNA-seq profiles of lung-resident ILCs at steady state and after in vivo stimulation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
770 Samples
Download data: MTX, TSV, TXT
Series
Accession:
GSE102299
ID:
200102299
8.

Core Binding Factor β Is Required For Group-2 Innate Lymphoid Cell Activation

(Submitter supplied) Group-2 innate lymphoid cells (ILC2) are tissue-resident, long-lived innate effector cells implicated in allergy and asthma. Upon activation, mature ILC2 rapidly secret large amounts of type-2 cytokines and other effector molecules. The molecular pathways that drive ILC2 activation are not well understood. Here we report that the transcriptional controller Core-binding factor β (CBFβ) is required for ILC2 activation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17791
6 Samples
Download data: CEL
Series
Accession:
GSE116062
ID:
200116062
9.

Induction of human regulatory innate lymphoid cells from group 2 innate lymphoid cells by retinoic acid

(Submitter supplied) We aimed to determine the characteristic of IL-10-producing ILCs induced from ILC2s by RA. We found that IL-10-producing ILCs has distinct characteristic compared to IL-10 negative ILCs.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT
10.

Gene expression data of naïve and activated ILC2s isolated from female and male mouse lungs

(Submitter supplied) Epidemiological studies have shown sex differences in prevalence of non-allergic asthma. Recent reports demonstrated negative effects of androgen signaling on group 2 innate lymphoid cells (ILC2s), explaining a potential mechanism behind sex bias in asthma prevalence. To further understand the difference in ILC2s based on sex, we have investigated the effects of sex and age on the number and function of lung ILC2s, and epithelium derived cytokines. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
12 Samples
Download data: CEL
Series
Accession:
GSE119350
ID:
200119350
11.

Expression data from WT and KO of Myc in innate lymphoid cell 2 (ILC2) in mice

(Submitter supplied) Group-2 innate lymphoid cells (ILC2) serve crucial function in allergy and asthma. Activated ILC2 rapidly proliferate and secret large amounts of type-2 cytokines, such as IL-5 and IL-13. Mechanisms underlying still remain ambiguous. Here we report that Myc is required for ILC2 proliferation and activation in allergic airway inflammation. Inhibition of Myc impair the ILC2 proliferation in vivo and prevented ILC2-mediated airway hyperresponsiveness in vivo. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17791
6 Samples
Download data: CEL
Series
Accession:
GSE129309
ID:
200129309
12.

Iron controls the development of airway hyperreactivity by regulating ILC2 metabolism and effector function

(Submitter supplied) Group 2 innate lymphoid cells (ILC2s) rapidly induce a type 2 inflammation in the lungs in response to allergens. Here, we focused on the role of iron – a critical nutritional trace element – on ILC2 function and asthma pathogenesis. In the lungs, transferrin receptor 1 (TfR1) is rapidly upregulated and functional during ILC2 activation, while blocking transferrin uptake reduces ILC2 expansion and activation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: TXT
Series
Accession:
GSE262210
ID:
200262210
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