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Links from GEO DataSets

Items: 20

1.

Transcription factor Bcl11b controls identity and function of mature innate lymphoid cells type II

(Submitter supplied) Type-2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies. Though Bcl11b has been previously considered a T-lineage identity transcription factor (TF) that restrains the innate-cell genetic programs, we report here that Bcl11b is highly expressed in mature ILC2s and acts upstream of the key ILC2 TFs Gfi1, Gata-3, and of IL-33 receptor IL1rl1 (T1ST2). Additionally, Bcl11b-/- ILC2s de-repressed Rorγt, Ahr and IL-23 receptor, normally expressed in type-3 ILCs (ILC3s). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
2 Samples
Download data: TXT
Series
Accession:
GSE67437
ID:
200067437
2.

Gut Adaptation of Ahr Expression Cell-intrinsically Restricts Group 2 Innate Lymphoid Cell Function

(Submitter supplied) Innate lymphoid cells (ILCs) are important for mucosal immunity. The intestine harbors all ILC subsets; however, how these cells orchestrate each other to achieve immune homeostasis and mount appropriate immunity during infection remains elusive. Here, we show that the adaptation of the aryl hydrocarbon receptor (Ahr) expression in the gut is a key regulatory mode for the host to keep the ILC balance. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
32 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE119461
ID:
200119461
3.

Specification of innate type-2 lymphocytes by the transcriptional determinant Gfi1

(Submitter supplied) Innate type-2 lymphoid cells (ILC2s) function in immune responses against helminth parasites and are implicated in allergic inflammation and asthma. ILC2s are activated by the epithelial-derived cytokines IL-33 and IL-25 and are major sources of the type-2 cytokines IL-5 and IL-13. We show that the transcription factor Gfi1 promotes the generation of ILC2s and controls their responsiveness during Nippostrongylus brasiliensis infection as well as IL-33- or IL-25-instigated inflammation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11002
2 Samples
Download data: CSV
Series
Accession:
GSE50806
ID:
200050806
4.

Mouse ILC2 cells from wild-type or Gfi1-KO animals

(Submitter supplied) Innate type-2 lymphocytes (ILC2s) are a newly described cell type whose biology and contribution to disease are poorly understood. We are interested in investigating the role of the transcription factor Gfi1 in ILC2s, which appear to be a prominent source of IL-5 and IL-13 during type-2 immune responses. We have compelling evidence demonstrating a critical role for Gfi1 in the development and effector state of ILC2s. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11202
7 Samples
Download data: TXT
Series
Accession:
GSE45621
ID:
200045621
5.

The transcription factor GATA3 is critical for the development of all IL-7Ra-expressing innate lymphoid cells (ILCs) and maintenance of type 2 ILCs

(Submitter supplied) Innate lymphoid cells (ILCs) play critical roles during innate immune responses to pathogens and lymphoid organ development. IL-7Ra+ ILC subsets, similar to T helper (Th) cell subsets, produce distinctive effector cytokines. The molecular control of IL-7Ra+ ILC development and maintenance has yet to be dissected. Here we report that GATA3 is indispensable for the development of all IL-7Ra+ ILC subsets and T cells. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BED
Series
Accession:
GSE47851
ID:
200047851
6.

Group 3 innate lymphoid cells continuously require the transcription factor GATA3 after commitment

(Submitter supplied) GATA3 is indispensable for the development of all IL-7Rα-expressing innate lymphoid cells (ILCs) and maintenance of type 1 ILCs (ILC1s) and type 2 ILCs (ILC2s). However, the importance of low GATA3 expression in type 3 ILCs (ILC3s) is still elusive. Here, we report that GATA3 regulates homeostasis of ILC3s by controlling IL-7Rα expression. In addition, GATA3 is critical for the development of NKp46+ ILC3 subset partially through regulating the balance between T-bet and RORγt. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
16 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE71198
ID:
200071198
7.

Bcl11b, a Novel GATA3-Interacting Protein, Suppresses Th1 while Limiting Th2 Cell Differentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL21493
35 Samples
Download data: TXT
Series
Accession:
GSE109109
ID:
200109109
8.

Bcl11b- and GATA3-mediated gene regulation in Th2 cells

(Submitter supplied) GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we report that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
19 Samples
Download data: TXT
Series
Accession:
GSE109107
ID:
200109107
9.

Bcl11b, a Novel GATA3-Interacting Protein, Suppresses Th1 while Limiting Th2 Cell Differentiation (H3K27ac and DNase-Seq)

(Submitter supplied) GATA-binding protein 3 (GATA3) acts as the master transcription factor for type 2 T helper (Th2) cell differentiation and function. However, it is still elusive how GATA3 function is precisely regulated in Th2 cells. Here, we report that the transcription factor B cell lymphoma 11b (Bcl11b), a previously unknown component of GATA3 transcriptional complex, is involved in GATA3-mediated gene regulation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21493
16 Samples
Download data: TXT
Series
Accession:
GSE108633
ID:
200108633
10.

Cell-type specific action of Bcl11b in early T-lineage and group 2 innate lymphoid cell

(Submitter supplied) The zinc finger transcription factor, Bcl11b, is expressed in T cells and group 2 innate lymphoid cells (ILC2s) among hematopoietic cells. In early T-lineage cells, Bcl11b directly binds and represses endogenous E protein antagonist, Id2, expression to prevent pro-T cell from adopting an innate-like fate. In contrast, ILC2s co-express both Bcl11b and Id2. Here, to address this contradiction, we have directly compared Bcl11b action mechanisms in pro-T cells and ILC2s. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
32 Samples
Download data: TXT
Series
Accession:
GSE131082
ID:
200131082
11.

CD4+ T-cells during Th2 immune responses

(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; Other
Platforms:
GPL17021 GPL19057
15 Samples
Download data: BW, TXT
Series
Accession:
GSE99599
ID:
200099599
12.

Transcriptome analysis of Bcl11b-deficient CD4+ T-cells during Th2 immune response

(Submitter supplied) Naïve CD4+ T-helper cells differentiate into Th2 effector cells during asthma and helminth (worm) infection. Here, we report that mice lacking the transcription factor Bcl11b in mature CD4+ T-cells are incapable of mounting an effective Th2 response in asthma and worm infection, with a major reduction of Th2 cytokine secretion and GATA3 expression. We found that Bcl11b exerts its role in Th2 differentiation through several avenues: (1) association with intronic regions at the Gata3 locus, sustaining GATA3 expression; (2) binding to and restricting chromatin accessibility at the Il4 silencer, located at hypersensitivity site (HS) IV; and (3) restricting Runx3 expression by association with a regulatory region 5’ of Runx3. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL19057
8 Samples
Download data: CSV, TXT
Series
Accession:
GSE99598
ID:
200099598
13.

Mapping of Bcl11b binding in CD4+ T-cells during Th2 immune response

(Submitter supplied) Naïve CD4+ T-helper cells differentiate into Th2 effector cells during asthma and helminth (worm) infection. Here, we report that mice lacking the transcription factor Bcl11b in mature CD4+ T-cells are incapable of mounting an effective Th2 response in asthma and worm infection, with a major reduction of Th2 cytokine secretion and GATA3 expression. We found that Bcl11b exerts its role in Th2 differentiation through several avenues: (1) association with intronic regions at the Gata3 locus, sustaining GATA3 expression; (2) binding to and restricting chromatin accessibility at the Il4 silencer, located at hypersensitivity site (HS) IV; and (3) restricting Runx3 expression by association with a regulatory region 5’ of Runx3. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
3 Samples
Download data: BW
Series
Accession:
GSE99597
ID:
200099597
14.

Genome wide mapping of accessible chromatin in CD4+ T-cells during Th2 immune responses

(Submitter supplied) Naïve CD4+ T-helper cells differentiate into Th2 effector cells during asthma and helminth (worm) infection. Here, we report that mice lacking the transcription factor Bcl11b in mature CD4+ T-cells are incapable of mounting an effective Th2 response in asthma and worm infection, with a major reduction of Th2 cytokine secretion and GATA3 expression. We found that Bcl11b exerts its role in Th2 differentiation through several avenues: (1) association with intronic regions at the Gata3 locus, sustaining GATA3 expression; (2) binding to and restricting chromatin accessibility at the Il4 silencer, located at hypersensitivity site (HS) IV; and (3) restricting Runx3 expression by association with a regulatory region 5’ of Runx3. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL19057
4 Samples
Download data: BW
Series
Accession:
GSE99595
ID:
200099595
15.

ILC2 development requires GATA3-related super-enhancers after lineage commitment

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below. Group 2 innate lymphoid cells (ILC2) are a subset of innate lymphocytes that produce type 2 cytokines, including IL-4, IL-5, and IL-13. GATA3 being a critical transcription factor for ILC2 development at multiple stages. However, when and how GATA3 is induced to the levels required for ILC2 development remains elusive. Herein, we identified ILC2-specific tandem GATA3-related super-enhancers (G3SE) that induce high GATA3 in ILC2-committed precursors. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL24247 GPL17021
17 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE218155
ID:
200218155
16.

Single cell RNA sequencing for α lymphoid progenitor

(Submitter supplied) The single-cell transcriptional analysis of bone marrow progenitors and subsequent analysis revealed that GATA3 induction in late ILC2-committed precursor depends on the G3SE lesion and that the upregulation of GATA3 in the late ILC2-precursor is required for the transition to mature ILC2.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: TXT, XLSX
Series
Accession:
GSE218154
ID:
200218154
17.

H3K27ac ChIP-seq for lung ILC2 and CD4 T cells in HDM induced asthma

(Submitter supplied) Lung ILC2 and Th2 cells exhibited similar chromatin activation. However, small fraction of super-enhancers showed ILC2-specific, or T cell specific activation.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: BEDGRAPH
Series
Accession:
GSE218144
ID:
200218144
18.

ATAC-seq of bone marrow ILC2 lineages and Lung ILC2 steady state

(Submitter supplied) ATAC-seq were performed for bone marrow ILC2 lineages and lung ILC2 of C57BL/6 mice and G3SEKO mice.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: BEDGRAPH
Series
Accession:
GSE218142
ID:
200218142
19.

Asynchronous combinatorial action of four regulatory factors activates Bcl11b for T cell commitment

(Submitter supplied) During T cell development, multipotent progenitors relinquish competence for other fates and commit to the T cell lineage by turning on Bcl11b, which encodes a transcription factor. To clarify lineage commitment mechanisms, we followed developing T cells at the single-cell level using Bcl11b knock-in fluorescent reporter mice. Notch signaling and Notch activated transcription factors collaborate to activate Bcl11b expression irrespectively of Notch-dependent proliferation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: FPKM_TRACKING
Series
Accession:
GSE76606
ID:
200076606
20.

Complementarity and redundancy of IL-22-producing innate lymphoid cells

(Submitter supplied) Homeostasis of the gut microbiota is pivotal to the survival of the host. Intestinal T cells and Innate Lymphoid cells (ILCs) control the composition of the microbiota and respond to its perturbations. Interleukin 22 (IL-22) plays a pivotal role in the immune control of gut commensal and pathogenic bacteria and is secreted by a heterogeneous population of intestinal T cells, NCR- ILC3 and NCR+ILC3. Expression of NCR by ILC3 is believed to define an irreversible effector ILC3 end-state fate in which these cells are key to control of bacterial infection via their production of IL-22. Here we identify the core transcriptional signature that drives the differentiation of NCR- ILC3 into NCR+ ILC3 and reveal that NCR+ILC3 exhibit more plasticity than originally thought, as NCR+ ILC3 can revert to NCR- ILC3. Contrary to the prevailing understanding of NCR+ ILC3 genesis and function, in vivo analyses of mice conditionally deleted of the key ILC3 genes Stat3, Il22, Tbet and Mcl1 demonstrated that NCR+ ILC3 were not essential for the control of colonic infections in the presence of T cells. However, NCR+ ILC3 were mandatory for homeostasis of the caecum. Our data identify that the interplay of intestinal T cells and ILC3 results in robust complementary fail-safe mechanisms that ensure gut homeostasis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
16 Samples
Download data: TXT
Series
Accession:
GSE72909
ID:
200072909
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