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Critical role of the transcription factors IRF1 and BATF in preparing the chromatin landscape during Type 1 regulatory cell differentiation [ATAC-seq]

ABSTRACT: Type 1 regulatory T (Tr1) cells are induced by interleukin-27 (IL-27) and have critical roles in the control of autoimmunity and resolution of inflammation. Here, we show that the transcription factors IRF1 and BATF are induced early during treatment with IL-27 and are required for the differentiation and function of Tr1 cells in vitro and in vivo. Epigenetic and transcriptional analyses reveal that both transcription factors influence chromatin accessibility and expression of genes required for Tr1 cell function. IRF1 and BATF deficiencies uniquely alter the chromatin landscape, suggesting that these factors serve a pioneering function during Tr1 cell differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE92993 | GEO | 2017/01/27

SECONDARY ACCESSION(S): PRJNA359391

REPOSITORIES: GEO

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Critical role of the transcription factors IRF1 and BATF in preparing the chromatin landscape during Type 1 regulatory cell differentiation [RNA-seq]

Project description:Type 1 regulatory T (Tr1) cells are induced by interleukin-27 (IL-27) and have critical roles in the control of autoimmunity and resolution of inflammation. Here, we show that the transcription factors IRF1 and BATF are induced early during treatment with IL-27 and are required for the differentiation and function of Tr1 cells in vitro and in vivo. Epigenetic and transcriptional analyses reveal that both transcription factors influence chromatin accessibility and expression of genes required for Tr1 cell function. IRF1 and BATF deficiencies uniquely alter the chromatin landscape, suggesting that these factors serve a pioneering function during Tr1 cell differentiation.

2017-01-27 | GSE92992 | GEO

Expression data for wildtype CD4+ T cells cells differentiated in Tr1 conditions for 2 hours

Project description:Type 1 regulatory T (Tr1) cells are induced by the interleukin-27 (IL-27) and have critical roles in the control of autoimmunity and resolution of inflammation. Here, we show that the transcription factors IRF1 and BATF are induced early during treatment with IL-27 and are required for the differentiation and function of Tr1 cells in vitro and in vivo . Epigenetic and transcriptional analyses reveal that both transcription factors influence chromatin accessibility and expression of genes required for Tr1 cell function. IRF1 and BATF deficiencies uniquely alter the chromatin landscape, suggesting that these factors serve a pioneering function during Tr1 cell differentiation.

2017-01-27 | GSE92940 | GEO

Critical role of the transcription factors IRF1 and BATF in preparing the chromatin landscape during Type 1 regulatory cell differentiation

Project description:Critical role of the transcription factors IRF1 and BATF in preparing the chromatin landscape during Type 1 regulatory cell differentiation

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Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (RNA-Seq)

Project description:Th17 cells secrete IL-17A, IL-17F, IL-21, and IL-22 cytokines that are critical in mediating inflammation and protecting the host from microorganisms infection. The basic leucine zipper transcription factor ATF-like (Batf) contributes to the transcriptional programming of multiple effector T cells, and is required for Th17 cell development. Here, we have interrogated mechanisms by which Batf promotes and stabilizes Th17 cell phenotype. We have shown that in vitro differentiated Th17 cells have increased expression of Th1 and Treg signature genes in the absence of Batf. In addition, Citrobacter rodentium infected Batf-deficient (Batf KO) mice fail to clear the infection, and that is correlated with diminished IL-17A and IL-22 cytokine production and increased Foxp3 and Ifng expression compared to WT mice. We find that Batf sustains Th17 phenotype in long-term culture conditions by suppressing Th1- and Treg-specific gene expression. Mechanistically, we reveal that Batf negatively regulates IL-2-STAT5 signaling and modulates STAT5 binding at the Ifng and Foxp3 gene loci thus suppressing Th1-Treg phenotype in Th17 cell development. Inhibition of STAT5 DNA binding activity in Batf KO Th17 cells was able to repress Ifng and Foxp3 expression compared to control-treated cells. Moreover, STAT5 cooperates with transcription factors Ets1 and Runx1 to mediate epigenetic modification and regulate gene expression. Thus, our study has revealed an essential function of Batf in modulating the IL-2-STAT5 signaling to promote and stabilize Th17 cell development.

2023-04-26 | GSE167418 | GEO

Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (ChIP-Seq)

2023-04-26 | GSE167417 | GEO

BATF-JUN is critical for IRF4-mediated transcription in T cells

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

Comparison of gene expression profiles of naÃ¯ve and in vitro effector CD8+ T cells from wild-type and BATF-/- mice

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. P14 TCR transgenic CD8+ T cells from wild-type or BATF-/- mice were examined either as naÃ¯ve cells or after 3 days of in vitro stimulation with antibodies to CD3 and CD28 in the presence of IL-2

2014-03-02 | E-GEOD-54215 | biostudies-arrayexpress

IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy

Project description:IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy

2021-07-03 | GSE179304 | GEO

BATF orchestrates the functional specification and metabolic reprogramming in Treg cells

Project description:Purpose: Identification of the differentially expressed genes and metabolic pathways in resting and activated WT and BATF-deficient Treg cells Methods: RNA was purified from resting of stimulated (aCD3-CD38/IL-2 for 48 h)Treg cells isolated from WT or Foxp3CreBatffl/fl mice Results: Loss of BATF promotes triacylglycerol biosynthesis in Treg cells. Conclusions: BATF is crucial to coordinate the suppressive function and triacylglycerol metabolism of Treg cells.

2021-03-02 | GSE149197 | GEO

Bach2-Batf interactions control Th2-type immune responses by regulating the IL-4 amplification loop

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

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