Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA264362 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1617100.fastq.gz | Fastqsanger.gz | |||
| SRR1617101.fastq.gz | Fastqsanger.gz | |||
| SRR1617102.fastq.gz | Fastqsanger.gz | |||
| SRR1617103.fastq.gz | Fastqsanger.gz | |||
| SRR1617104.fastq.gz | Fastqsanger.gz |
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Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.
2024-03-05 | PXD041987 | Pride
Project description:Interferon regulatory factor 4 (IRF4) is an IRF family transcription factor with critical roles in lymphoid development and in regulating the immune response. IRF4 binds DNA weakly owing to a carboxy-terminal auto-inhibitory domain, but cooperative binding with factors such as PU.1 or SPIB in B cells increases binding affinity, allowing IRF4 to regulate genes containing ETS–IRF composite elements (EICEs; 5'-GGAAnnGAAA-3'). Here we show that in mouse CD4+ T cells, where PU.1/SPIB expression is low, and in B cells, where PU.1 is well expressed, IRF4 unexpectedly can cooperate with activator protein-1 (AP1) complexes to bind to AP1–IRF4 composite (5'-TGAnTCA/GAAA-3') motifs that we denote as AP1–IRF composite elements (AICEs). Moreover, BATF–JUN family protein complexes cooperate with IRF4 in binding to AICEs in pre-activated CD4+ T cells stimulated with IL-21 and in TH17 differentiated cells. Importantly, BATF binding was diminished in Irf4-/- T cells and IRF4 binding was diminished in Batf-/- T cells, consistent with functional cooperation between these factors. Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in TH17 cells and potently regulated by IL-21. These findings reveal that IRF4 can signal via complexes containing ETS or AP1 motifs depending on the cellular context, thus indicating new approaches for modulating IRF4-dependent transcription. Genome-wide transcription factors mapping and binding of IRF4, BATF, IRF8, STAT3, JUN etc in WT, Irf4-/- and Batf-/- mice in different cell types (B cells, CD4+ T cells and TH17 cells) cultured with or without IL-21 was conducted. RNA-Seq is conducted in mouse B cells, CD4+ T cells, TH1/TH2/TH9/TH17/Treg.
2012-09-18 | E-GEOD-39756 | biostudies-arrayexpress
Project description:Although Bach2 plays an important role in regulating the Th2-type immune response, the underlying molecular mechanisms remain unclear. We herein demonstrate that Bach2 associates with Batf and binds to the regulatory regions of the Th2 cytokine gene loci. The Bach2-Batf complex antagonizes the recruitment of the Batf-Irf4 complex to AP-1 motifs and suppresses Th2 cytokine production. Furthermore, we found that Bach2 regulates the Batf and Batf3 expressions via two distinct pathways. First, Bach2 suppresses the maintenance of the Batf and Batf3 expression through the inhibition of IL-4 production. Second, the Bach2-Batf complex directly binds to the Batf and Batf3 gene loci and reduces transcription by interfering with the Batf-Irf4 complex. These findings suggest that IL-4 and Batf form a positive feedback amplification loop to induce Th2 cell differentiation and the subsequent Th2-type immune response, and Bach2-Batf interactions are required to prevent an excessive Th2 response.
2016-11-14 | GSE65084 | GEO
Project description:Purpose: The purpose of this study is to identify the genome-wide binding sites for IRF4 interaction partners PU.1, BATF, and JunB in dendritic cells. These ChIP-seq data were integrated with gene expression analysis in IRF4-sufficient and -deficient BMDCs in order to assemble an IRF4 gene regulatory network. Hematopoietic bone marrow progenitors from C57BL/6 mice were differentiated with GM-CSF and IL-4 for 5 days. On day 6, BMDCs were stimulated for 6 hours with 100ng/ml LPS. Fixed chromatin was immunoprecipitated with anti-PU.1, BATF, and JunB antibodies and subjected to high-throughput sequencing. The sequencing data for the input DNA was previously submitted as GSM999807.
2013-12-22 | E-GEOD-52772 | biostudies-arrayexpress
Project description:Studies over the past decade characterized murine regulatory T cells (Tregs) with the capacity to promote tissue regeneration. In humans, such a population of tissue-repair Treg cells has not been discovered yet. Using single-cell chromatin accessibility profiles of murine and human tissue Treg cells, we defined a species-conserved and microbiota-independent repair Treg signature, with a prevailing footprint of the transcription factor BATF. Combining this signature with gene expression profiling and TCR fate mapping, we identified a population of tissue-like Treg cells in peripheral blood, characterized by the expression of BATF, CCR8 and HLA-DR. Human BATF+CCR8+ Treg cells from normal skin and adipose tissue shared features with tumor-resident Treg and tissue T-follicular helper (Tfh) cells. Inducing a Tfh-like differentiation program in naive Treg cells partially recapitulated human tissue Treg characteristics, including enhanced wound healing potential
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Project description:The transcription factor BATF plays critical roles in the differentiation of various immune cells, including CD8+ T cells. Here, we demonstrated that BATF controls epigenomic and transcriptomic reprogramming of CD8+ T cells at an early phase of acute viral infection, thereby promoting the differentiation of cytolytic effector CD8+ T cells. Loss of BATF drastically perturbed gene expression, chromatin accessibility, and the bindings of key transcription factors including Jun, T-bet, and IRF4. The direct interaction with IRF4 was essential for BATF-mediated effector differentiation, as the BATF mutant lacking this interaction failed to induce proper chromatin remodeling and proliferation of antigen-specific CD8+ T cells. Notably, IRF4 binding was exhaustively dependent on BATF, whereas BATF retained binding capacity even in IRF4-deficient CD8+ T cells. Furthermore, BATF initiated chromatin remodeling in the absence of IRF4, whereas subsequent dynamic epigenomic reorganization required IRF4. Our data proposed that BATF serves as a “pioneer transcription factor” spearheading the reorganization of chromatin architecture upon antigen encounter, followed by further rearrangement of epigenomic and transcriptomic landscapes through the cooperation with IRF4.
2025-07-09 | GSE281499 | GEO
Project description:The transcription factor BATF plays critical roles in the differentiation of various immune cells, including CD8+ T cells. Here, we demonstrated that BATF controls epigenomic and transcriptomic reprogramming of CD8+ T cells at an early phase of acute viral infection, thereby promoting the differentiation of cytolytic effector CD8+ T cells. Loss of BATF drastically perturbed gene expression, chromatin accessibility, and the bindings of key transcription factors including Jun, T-bet, and IRF4. The direct interaction with IRF4 was essential for BATF-mediated effector differentiation, as the BATF mutant lacking this interaction failed to induce proper chromatin remodeling and proliferation of antigen-specific CD8+ T cells. Notably, IRF4 binding was exhaustively dependent on BATF, whereas BATF retained binding capacity even in IRF4-deficient CD8+ T cells. Furthermore, BATF initiated chromatin remodeling in the absence of IRF4, whereas subsequent dynamic epigenomic reorganization required IRF4. Our data proposed that BATF serves as a “pioneer transcription factor” spearheading the reorganization of chromatin architecture upon antigen encounter, followed by further rearrangement of epigenomic and transcriptomic landscapes through the cooperation with IRF4.
2025-07-09 | GSE281498 | GEO
Project description:The transcription factor BATF plays critical roles in the differentiation of various immune cells, including CD8+ T cells. Here, we demonstrated that BATF controls epigenomic and transcriptomic reprogramming of CD8+ T cells at an early phase of acute viral infection, thereby promoting the differentiation of cytolytic effector CD8+ T cells. Loss of BATF drastically perturbed gene expression, chromatin accessibility, and the bindings of key transcription factors including Jun, T-bet, and IRF4. The direct interaction with IRF4 was essential for BATF-mediated effector differentiation, as the BATF mutant lacking this interaction failed to induce proper chromatin remodeling and proliferation of antigen-specific CD8+ T cells. Notably, IRF4 binding was exhaustively dependent on BATF, whereas BATF retained binding capacity even in IRF4-deficient CD8+ T cells. Furthermore, BATF initiated chromatin remodeling in the absence of IRF4, whereas subsequent dynamic epigenomic reorganization required IRF4. Our data proposed that BATF serves as a “pioneer transcription factor” spearheading the reorganization of chromatin architecture upon antigen encounter, followed by further rearrangement of epigenomic and transcriptomic landscapes through the cooperation with IRF4.
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Project description:This SuperSeries is composed of the following subset Series: GSE40726: Transcriptional profiling of IRF4 -/- vs IRF4 +/- T-cells under Th17 polarizing conditions GSE40727: ChIPseq analysis of IRF4 and BATF in immune cells Refer to individual Series
2012-09-13 | E-GEOD-40483 | biostudies-arrayexpress
Project description:We identify a subset of IL-33 expressing adventitial stromal cells as local regulators of ILC2s Type 2 lymphocytes promote both physiologic tissue remodeling and allergic pathology, yet their physical tissue niches are poorly described. In this study, we used quantitative imaging together with scRNAseq to define tissue niches of group 2 innate lymphoid cells (ILC2s), critical instigators of type 2 immunity. We identified a dominant adventitial cuff niche around lung bronchi and larger vessels in multiple tissues, where ILC2s localized with subsets of dendritic and regulatory T cells. However, ILC2s were most intimately associated with adventitial stromal cells (ASC), a mesenchymal fibroblast-like subset that expressed Interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP) and supported ILC2s and tissue-resident Th2 cells.
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